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1
Arnaud, Philippe. "Genomic imprinting in germ cells: imprints are under control." REPRODUCTION 140, no. 3 (September 2010): 411–23. http://dx.doi.org/10.1530/rep-10-0173.
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The cis-acting regulatory sequences of imprinted gene loci, called imprinting control regions (ICRs), acquire specific imprint marks in germ cells, including DNA methylation. These epigenetic imprints ensure that imprinted genes are expressed exclusively from either the paternal or the maternal allele in offspring. The last few years have witnessed a rapid increase in studies on how and when ICRs become marked by and subsequently maintain such epigenetic modifications. These novel findings are summarised in this review, which focuses on the germline acquisition of DNA methylation imprints and particularly on the combined role of primary sequence specificity, chromatin configuration, non-histone proteins and transcriptional events.
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Smolinska-Kempisty, Katarzyna, Joanna Wolska, and Marek Bryjak. "Molecularly Imprinting Microfiltration Membranes Able to Absorb Diethyl Phthalate from Water." Membranes 12, no. 5 (May 8, 2022): 503. http://dx.doi.org/10.3390/membranes12050503.
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In this study, polypropylene porous membranes with an average pore size of 1.25 µm were modified by barrier discharge plasma. Next, molecularly imprinted layers with an imprint of diethyl phthalate (DEP) ware grafted of their surface. In order to optimize the composition of the modifying mixture various solvents, the ratios of functional monomers and the cross-linking monomer as well as various amounts of phthalate were verified. It was shown that the most effective membranes were obtained during polymerization in n-octane with the participation of functional monomers in the ratio 3:7 and the amount of phthalate 7 wt.%. The membranes were tested in the filtration process as well as static and dynamic sorption. In all of these processes, the imprinted membranes showed better properties than those without the imprint. The diethyl phthalate retention coefficient was 36.12% for membranes with a grafting yield of 1.916 mg/cm2. On the other hand, DEP static sorption for the imprinted membranes was 3.87 µmol/g higher than for non-imprinted membranes. Also, in the process of dynamic sorption higher values were observed for membranes with the imprint (DSMIM, 4.12 µmol/g; DSNIM, 1.18 µmol/g). The membranes were also tested under real conditions. In the process of filtration of tap water contaminated with phthalate, the presence of imprints in the membrane structure resulted in more than three times higher sorption values (3.09 µmol/g) than in the case of non-imprinted membranes (1.12 µmol/g).
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Nykänen, Nooa. "Following the Old Road: Organizational Imprinting and the Regional Development of Russia." Management and Organization Review 17, no. 3 (May 19, 2021): 583–616. http://dx.doi.org/10.1017/mor.2020.83.
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ABSTRACTIn this article, I draw from organizational imprinting theory to illuminate the impact of the Soviet legacy on contemporary Russian economic geography and regional policy. I argue that central coordination in the creation and regulation of Russian urban agglomerations is connected to a socialist imprinted paradigm associated with the Soviet economic regionalization model and territorial-production complexes (TPCs). I conduct a qualitative historical study to analyze the role of the foundational environment and the dynamics in the development of this imprint. I propose that this imprint effect is prone to reproduction in contemporary regional development strategies and community-based paradigms due to exaptation and cultural-cognitive persistence. The article extends the literature of socialist imprinting by demonstrating how imprints may emerge, transform, and affect localized organizational communities in transition economies and highlights the role of imprinted paradigms in policymaking and regional development.
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O'Doherty, A. M., D. Magee, M. E. Beltman, S. Mamo, D. Rizos, and T. Fair. "88 VARIABLE DNA METHYLATION PROFILES AT IMPRINTED LOCI IN BOVINE EARLY PRE-IMPLANTATION EMBRYOS." Reproduction, Fertility and Development 25, no. 1 (2013): 192. http://dx.doi.org/10.1071/rdv25n1ab88.
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The DNA methylation imprints, at maternally imprinted gene differentially methylated regions, are established during the postnatal growth stage of oogenesis, with paternal imprints being acquired in the perinatal prospermatagonia. Murine DNA methylation marks, at imprinted loci, are widely regarded to be resistant to post-fertilization demethylation events that occur in the paternal pronucleus of the zygote and to passive demethylation of the maternally derived genomic content from cleavage to the 16-cell stage. However, the DNA methylation profile of bovine imprinted genes following fertilization remains unknown. The objective of the current study was to analyze the methylation dynamics at several imprinted gene differentially methylated regions during bovine embryo development. In addition, a previously published RNA-seq database (Mamo et al. 2011 Biol. Reprod.) was mined for transcript abundance of genes associated with establishing and maintaining genomic imprints. Single in vivo blastocysts (Day 7), hatched ovoid embryos (Day 14), filamentous embryos (Day 17), and implanting conceptii (Day 25) were collected (n = 4–9, per time point) from beef heifers. Genomic DNA was isolated and bisulfite modified, using the EZ DNA methylation direct kit (Zymo, Irvine, CA, USA), and used as template in bisulfite PCR reactions. The PCR products were verified by agarose gel electrophoresis and subsequently pyrosequenced. Observed methylation values were most highly variable in Day 7 blastocysts, with values ranging between 13 and 44% (IGF2R), 5 and 63% (PEG10), 7 and 59% (MEST), 3 and 61% (SNRPN), 12 and 64% (PLAGL1), and 20 and 32% (H19). There was a marked reduction in variability as embryonic development progressed, with values at Day 25 ranging from 37 to 41% (IGF2R), 34 to 38% (PEG10), 31 to 37% (MEST), 36 to 40% (SNRPN), 17 to 26% (PLAGL1), and 25 to 30% (H19). Statistical analysis (Levene’s test for equal variance) of methylation values for each gene at each time point confirmed that the methylation values observed in Day 7 embryos were significantly variable (P < 0.05) when compared with later developmental stages. Concordant with this finding, RNA transcript levels of associated methylation machinery genes DNMT3A, DNMT3B, and TRIM28 progressively increased from Day 7 to 13 and subsequently decreased from Day 13 to 16. Taken together our results demonstrate that in cattle DNA methylation marks, at imprinted loci, are highly variable at the blastocyst stage and are progressively stabilized with increasing days post-fertilization. This stabilization of imprint is coordinated with a window of increased levels of associated methylation machinery transcripts. Work presented here provides evidence of a novel mechanism for bovine embryonic DNA methylation imprint maintenance. This work was funded by SFI grant number 07/SRC/B1156.
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Kato, Y., W. M. Rideout, K. Hilton, S. C. Barton, Y. Tsunoda, and M. A. Surani. "Developmental potential of mouse primordial germ cells." Development 126, no. 9 (May 1, 1999): 1823–32. http://dx.doi.org/10.1242/dev.126.9.1823.
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There are distinctive and characteristic genomic modifications in primordial germ cells that distinguish the germ cell lineage from somatic cells. These modifications include, genome-wide demethylation, erasure of allele-specific methylation associated with imprinted genes, and the re-activation of the X chromosome. The allele-specific differential methylation is involved in regulating the monoallelic expression, and thus the gene dosage, of imprinted genes, which underlies functional differences between parental genomes. However, when the imprints are erased in the germ line, the parental genomes acquire an equivalent epigenetic and functional state. Therefore, one of the reasons why primordial germ cells are unique is because this is the only time in mammals when the distinction between parental genomes ceases to exist. To test how the potentially imprint-free primordial germ cell nuclei affect embryonic development, we transplanted them into enucleated oocytes. Here we show that the reconstituted oocyte developed to day 9.5 of gestation, consistently as a small embryo and a characteristic abnormal placenta. The embryo proper also did not progress much further even when the inner cell mass was ‘rescued’ from the abnormal placenta by transfer into a tetraploid host blastocyst. We found that development of the experimental conceptus was affected, at least in part, by a lack of gametic imprints, as judged by DNA methylation and expression analysis of several imprinted genes. The evidence suggests that gametic imprints are essential for normal development, and that they can neither be initiated nor erased in mature oocytes; these properties are unique to the developing germ line.
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Vu, Hoang Yen, and A. N. Zyablov. "Determination of preservatives in liquids by piezosensors." Аналитика и контроль 26, no. 2 (2022): 134–40. http://dx.doi.org/10.15826/analitika.2022.26.2.001.
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In the current study, piezosensors based on the molecularly imprinted polyimides with imprints of potassium sorbate and sodium benzoate were obtained. Molecularly Imprinted Polymers (MIPs) were synthesized using a polyimide and a non-covalent imprinting technique. It was established that the use of 0.1 g/mL template concentration at the thermochemical stage led to the formation of the maximum number of molecular imprints on the film surface. Using the scanning force microscopy, it was found that the reference polymer film had a uniform surface with a small height difference from 1.4 to 2.6 nm (including 88.94 % of pores with a radius of up to 10 nm) and had good film thickness reproducibility. The surface morphology of films of molecularly imprinted polymers with imprints of potassium sorbate and sodium benzoate had more developed surface, which was associated with the peculiarities of the formation of imprints. In this work, imprinting factor (IF) and selectivity coefficient (k) of the sensor were calculated. Molecularly imprinted polymers had better selectivity, sensitivity, and ability to recognize target template molecules than the reference polymers (non-imprinted polymers). Molecularly imprinted polymer-modified piezoelectric sensors (MIP sensors) have been used to analyze potassium sorbate and sodium benzoate in non-alcoholic drinks. The linear concentration range was identified to be 5 - 500 mg/L and the limit of detection for potassium sorbate and sodium benzoate were 1.6 mg/L and 2 mg/L, respectively. The determination of potassium sorbate and sodium benzoate in non-alcoholic drinks was carried out by MIP sensors and spectrophotometry method. The results obtained by the sensors and the spectrophotometry method were in good agreement. The concentration of preservatives for the potassium sorbate and the sodium benzoate in non-alcoholic drinks was 130 - 176 mg/L and 129 - 146 mg/L, respectively.
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Edwards, Carol A., Nozomi Takahashi, Jennifer A. Corish, and Anne C. Ferguson-Smith. "The origins of genomic imprinting in mammals." Reproduction, Fertility and Development 31, no. 7 (2019): 1203. http://dx.doi.org/10.1071/rd18176.
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Genomic imprinting is a process that causes genes to be expressed according to their parental origin. Imprinting appears to have evolved gradually in two of the three mammalian subclasses, with no imprinted genes yet identified in prototheria and only six found to be imprinted in marsupials to date. By interrogating the genomes of eutherian suborders, we determine that imprinting evolved at the majority of eutherian specific genes before the eutherian radiation. Theories considering the evolution of imprinting often relate to resource allocation and recently consider maternal–offspring interactions more generally, which, in marsupials, places a greater emphasis on lactation. In eutherians, the imprint memory is retained at least in part by zinc finger protein 57 (ZFP57), a Kruppel associated box (KRAB) zinc finger protein that binds specifically to methylated imprinting control regions. Some imprints are less dependent on ZFP57invivo and it may be no coincidence that these are the imprints that are found in marsupials. Because marsupials lack ZFP57, this suggests another more ancestral protein evolved to regulate imprints in non-eutherian subclasses, and contributes to imprinting control in eutherians. Hence, understanding the mechanisms acting at imprinting control regions across mammals has the potential to provide valuable insights into our understanding of the origins and evolution of genomic imprinting.
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Tunster, S. J., A. B. Jensen, and R. M. John. "Imprinted genes in mouse placental development and the regulation of fetal energy stores." REPRODUCTION 145, no. 5 (May 2013): R117—R137. http://dx.doi.org/10.1530/rep-12-0511.
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Imprinted genes, which are preferentially expressed from one or other parental chromosome as a consequence of epigenetic events in the germline, are known to functionally converge on biological processes that enablein uterodevelopment in mammals. Over 100 imprinted genes have been identified in the mouse, the majority of which are both expressed and imprinted in the placenta. The purpose of this review is to provide a summary of the current knowledge regarding imprinted gene function in the mouse placenta. Few imprinted genes have been assessed with respect to their dosage-related action in the placenta. Nonetheless, current data indicate that imprinted genes converge on two key functions of the placenta, nutrient transport and placental signalling. Murine studies may provide a greater understanding of certain human pathologies, including low birth weight and the programming of metabolic diseases in the adult, and complications of pregnancy, such as pre-eclampsia and gestational diabetes, resulting from fetuses carrying abnormal imprints.
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MacDonald, William A. "Epigenetic Mechanisms of Genomic Imprinting: Common Themes in the Regulation of Imprinted Regions in Mammals, Plants, and Insects." Genetics Research International 2012 (February 15, 2012): 1–17. http://dx.doi.org/10.1155/2012/585024.
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Genomic imprinting is a form of epigenetic inheritance whereby the regulation of a gene or chromosomal region is dependent on the sex of the transmitting parent. During gametogenesis, imprinted regions of DNA are differentially marked in accordance to the sex of the parent, resulting in parent-specific expression. While mice are the primary research model used to study genomic imprinting, imprinted regions have been described in a broad variety of organisms, including other mammals, plants, and insects. Each of these organisms employs multiple, interrelated, epigenetic mechanisms to maintain parent-specific expression. While imprinted genes and imprint control regions are often species and locus-specific, the same suites of epigenetic mechanisms are often used to achieve imprinted expression. This review examines some examples of the epigenetic mechanisms responsible for genomic imprinting in mammals, plants, and insects.
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Csaba, György. "Hormonal imprinting in the central nervous system: causes and consequences." Orvosi Hetilap 154, no. 4 (January 2013): 128–35. http://dx.doi.org/10.1556/oh.2013.29533.
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The notion of the perinatal „hormonal imprinting” has been published at first in 1980 and since that time it spred expansively. The imprintig develops at the first encounter between the developing receptor and the target hormone – possibly by the alteration of the methylation pattern of DNA – and it is transmitted to the progeny generations of the cell. This is needed for the complete development of the receptor’s binding capacity. However, molecules similar to the target hormone (hormone-analogues, drugs, chemicals, environmental pollutants) can also bind to the developing receptor, causing faulty imprinting with life-long consequences. This can promote pathological conditions. Later it was cleared that in other critical periods such as puberty, imprinting also can be provoked, even in any age in differentiating cells. The central nervous system (brain) also can be mistakenly imprinted, which durably influences the dopaminergic, serotonergic and noradrenergic system and this can be manifested – in animal experiments – in alterations of the sexual and social behavior. In our modern age the faulty hormonal imprintig is inavoidable because of the mass of medicaments, chemicals, the presence of hormone-like materials (e.g. soya phytosteroids) in the food, and environmental pollutants. The author especially emphasizes the danger of oxytocin, as a perinatal imprinter, as it is used very broadly and can basically influence the emotional and social spheres and the appearance of certain diseases such as auitism, schizophrenia and parkinsonism. The danger of perinatal imprinters is growing, considering their effects on the human evolution. Orv. Hetil., 2013, 154, 128–135.
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Webster, K. E., M. K. O'Bryan, U. Aapola, P. E. Crewther, R. Lyle, S. J. Meachem, S. E. Antonarakis, et al. "255.Dnmt3L: a coordinator of epigenetic modifications during spermatogenesis." Reproduction, Fertility and Development 16, no. 9 (2004): 255. http://dx.doi.org/10.1071/srb04abs255.
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Spermatogenesis is a process with unique epigenetic requirements. The differentiation from diploid spermatogonia to haploid spermatozoa requires regulation of genomic imprint establishment, stage specific gene expression, meiotic division, and the histone-protamine transition. The methyltransferase regulator, Dnmt3L, is expressed during gametogenesis and is necessary for establishment of maternal methylation imprints in the oocyte. Targeted disruption of Dnmt3L does not appear to affect oogenesis, as mature oocytes are generated, however resultant heterozygous progeny die mid gestation due to biallelic expression of imprinted genes. Dnmt3L–/– males however show spermatogenic arrest. We found that this arrest occurs during prophase I of meiosis, with spermatocytes lost by both apoptosis and germ cell sloughing. A progressive degeneration ensues, resulting in a Sertoli cell phenotype. Electron microscopy of meiotic spermatocytes revealed that homologous chromosomes fail to align and form synaptonemal complexes. Furthermore, Dnmt3L–/– spermatocytes show abnormal methylation on paternally imprinted genes and abnormal global retention of histone acetylation, implicating Dnmt3L in histone deacetylase recruitment. Thus, during spermatogenesis, Dnmt3L is crucial for two distinct epigenetic modifications; imprint establishment and global histone deacetylation prior to homologous chromosome alignment. The latter defect is likely to affect the alignment of homologous chromosomes and trigger the pachytene checkpoint leading to spermatocyte death. Since Dnmt3L has no DNA methlytransferase or HDAC activity itself, we propose that Dnmt3L is essential for the coordination of epigenetic layers, at least during spermatogenesis.
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Kono, Tomohiro. "Genetic modification for bimaternal embryo development." Reproduction, Fertility and Development 21, no. 1 (2009): 31. http://dx.doi.org/10.1071/rd08213.
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Full mammalian development typically requires genomes from both the oocyte and spermatozoon. Biparental reproduction is necessary because of parent-specific epigenetic modification of the genome during gametogenesis; that is, a maternal methylation imprint imposed during the oocyte growth period and a paternal methylation imprint imposed in pregonadal gonocytes. This leads to unequivalent expression of imprinted genes from the maternal and paternal alleles in embryos and individuals. It is possible to hypothesise that the maternal methylation imprint is necessary to prevent parthenogenesis, which extinguishes the opportunity for having descendents, whereas the paternal methylation imprint prevents parthenogenesis, ensuring that a paternal contribution is obligatory for any descendants. To date, there are several lines of direct evidence that the epigenetic modifications that occur during oocyte growth have a decisive effect on mammalian development. Using bimaternal embryos with two sets of maternal genomes, the present paper illustrates how parental methylation imprints are an obstacle to the progression of parthenogenesis.
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Smith, A. "Why is There No Diploid Overdose Effect in Prader-Willi Syndrome Due to Uniparental Disomy?" Acta geneticae medicae et gemellologiae: twin research 45, no. 1-2 (April 1996): 179–89. http://dx.doi.org/10.1017/s0001566000001288.
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AbstractDue to DNA technology, it is now apparent that the mechanisms of genetic disease are more complex than the model of a gene with biallelic expression in the diploid state. If a gene is imprinted, monoallelic expression is the norm when the chromosomes of a pair are inherited normally from each parent. Uniparental disomy (UPD) is the abnormal situation where both chromosomes of a pair come from the same parent. When the chromosome contains an imprinted gene, UPD may result in nullisomy or disomy for a functional copy of that gene. If there are two imprinted loci on the same chromosome, UPD for that chromosome results in nullisomy for one imprinted gene but functional disomy for the other a “diploid overdose” (DO). This situation has been well demonstrated in the Prader-Willi syndrome (PWS) which is the nullisomic phenotype for the PWS gene(s) on chromosome 15q 11-13. Chromosome 15q11-13 also contains the gene for Angelman syndrome (AS) which has a phenotype distinct from PWS. Both loci are subject to imprinting – in PWS, the imprint is on the maternal chromosome 15, in AS it is on the paternal chromosome 15. All individuals with PWS due to maternal UPD, while functionally nullisomic for the PWS locus, are functionally disomic for the AS locus – a DO situation. Assuming that biallelic expression of an imprinted gene is harmful, one would expect DO for an imprinted gene to produce a phenotypic effect. Cases of PWS due to UPD do not appear to differ from those due to deletion (hypopigmentation in deletional cases can be explained by loss of D15S12 downstream from the critical region). There is no good evidence of DO for the AS locus in PWS due to UPD. Why then was it ‘necessary’ in evolutionary terms to imprint the AS locus and maintain the imprint faithfully for life. A similar situation of two imprinted genes on the same chromosome occurs with IGF2 and H19 on chromosome 11p15. Maternal imprinting for IGF2 and paternal imprinting for H19 is the norm. Paternal UPD in this situation does lead to a DO effect, namely Beckwith-Wiedemann syndrome. The possibility of a DO effect needs to be considered when assessing the phenotypic spectrum of UPD for other chromosomes currently under investigation.
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Nicholls, R. D., M. T. C. Jong, C. C. Glenn, J. Gabriel, P. K. Rogan, D. J. Driscoll, and S. Saitoh. "Multiple Imprinted Genes Associated with Prader-Willi Syndrome and Location of an Imprinting Control Element." Acta geneticae medicae et gemellologiae: twin research 45, no. 1-2 (April 1996): 87–89. http://dx.doi.org/10.1017/s000156600000115x.
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Our studies aim to identify the mechanisms and genes involved in genomic imprinting in mammalian development and human disease. Imprinting refers to an epigenetic modification of DNA that results in parent-of-origin specific expression during embryogenesis and in the adult. This imprint is reset at each generation, depending on the sex of the parental gametogenesis. Prader-Willi (PWS) and Angelman (AS) syndromes are excellent models for the study of genomic imprinting in humans, since these distinct neurobehavioural disorders are both associated with genetic abnormalities (large deletions, uniparental disomy, and imprinting mutations) of inheritance in chromosome 15q11-q13, dependent on the parental origin (reviewed in ref. 1). Some AS patients have biparental inheritance, consistent with a single imprinted gene (active on the maternal chromosome), whereas similar PWS patients are not found suggesting that at least two imprinted genes (active on the paternal allele) may be necessary for classical PWS. We have previously shown that the small ribonucleoprotein associated protein SmN gene (SNRPN), located in the PWS critical region [2], is only expressed from the paternal allele and is differentially methylated on parental alleles [3]. Therefore, SNRPN may have a role in PWS. Methylation imprints have also been found at two other loci in 15q11-q13, PW71 [4] and D15S9 [5], which map 120 kb and 1.5 Mb proximal to SNRPN, respectively. We have now characterized in detail the gene structure and expression from two imprinted loci within 15q11-q13, SNRPN and D15S9, which suggests that both loci are surprisingly complex, with important implications for the pathogenesis of PWS.
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Allen, Nick, and Wolf Reik. "What the papers say. Imprintor or imprinted?" BioEssays 14, no. 12 (December 1992): 857–59. http://dx.doi.org/10.1002/bies.950141211.
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Sleutels, Frank, and Denise P. Barlow. "Investigation of Elements Sufficient To Imprint the Mouse Air Promoter." Molecular and Cellular Biology 21, no. 15 (August 1, 2001): 5008–17. http://dx.doi.org/10.1128/mcb.21.15.5008-5017.2001.
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ABSTRACT Imprinted maternal-allele-specific expression of the mouse insulin-like growth-factor type 2 receptor (Igf2r) gene depends on a 3.7-kb element named region 2, located in the second intron of the gene. Region 2 carries a maternal-allele-specific methylation imprint and contains an imprinted CpG island promoter (Air) that expresses a noncoding antisense RNA from the paternal inherited allele only. Here, we use transgenes to test the minimal requirements for imprinting of Air and to test if the action of region 2 is restricted to Igf2r. Transgenes up to 9 kb with Air as a single promoter are expressed but not imprinted. When coupled to the Igf2rCpG island promoter on a 44-kb transgene, Air was imprinted in one of three lines. However, Air on a 4.6-kb fragment is also imprinted in 2 of 14 lines when inserted in an intron of an adenine phosphoribosyltransferase (Aprt) transgene, and in one line, the imprinted methylation and expression ofAir have been transferred onto the AprtCpG island promoter. These data suggest that a dual CpG island promoter setting may facilitate Air imprinting as a short transgene and also show that Air can transfer imprinting onto other genes. However, for reliable Air imprinting, elements are necessary that are located outside a 44-kb region spanning the Air-Igf2r promoters.
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Menheniott, Trevelyan R., Kathryn Woodfine, Reiner Schulz, Andrew J. Wood, David Monk, Andrew S. Giraud, H. Scott Baldwin, Gudrun E. Moore, and Rebecca J. Oakey. "Genomic Imprinting of Dopa decarboxylase in Heart and Reciprocal Allelic Expression with Neighboring Grb10." Molecular and Cellular Biology 28, no. 1 (October 29, 2007): 386–96. http://dx.doi.org/10.1128/mcb.00862-07.
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ABSTRACT By combining a tissue-specific microarray screen with mouse uniparental duplications, we have identified a novel imprinted gene, Dopa decarboxylase (Ddc), on chromosome 11. Ddc_exon1a is a 2-kb transcript variant that initiates from an alternative first exon in intron 1 of the canonical Ddc transcript and is paternally expressed in trabecular cardiomyocytes of the embryonic and neonatal heart. Ddc displays tight conserved linkage with the maternally expressed and methylated Grb10 gene, suggesting that these reciprocally imprinted genes may be coordinately regulated. In Dnmt3L mutant embryos that lack maternal germ line methylation imprints, we show that Ddc is overexpressed and Grb10 is silenced. Their imprinting is therefore dependent on maternal germ line methylation, but the mechanism at Ddc does not appear to involve differential methylation of the Ddc_exon1a promoter region and may instead be provided by the oocyte mark at Grb10. Our analysis of Ddc redefines the imprinted Grb10 domain on mouse proximal chromosome 11 and identifies Ddc_exon1a as the first example of a heart-specific imprinted gene.
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Prawitt, Dirk, and Thomas Haaf. "Basics and disturbances of genomic imprinting." Medizinische Genetik 32, no. 4 (November 18, 2020): 297–304. http://dx.doi.org/10.1515/medgen-2020-2042.
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Abstract Genomic imprinting ensures the parent-specific expression of either the maternal or the paternal allele, by different epigenetic processes (DNA methylation and histone modifications) that confer parent-specific marks (imprints) in the paternal and maternal germline, respectively. Most protein-coding imprinted genes are involved in embryonic growth, development, and behavior. They are usually organized in genomic domains that are regulated by differentially methylated regions (DMRs). Genomic imprints are erased in the primordial germ cells and then reset in a gene-specific manner according to the sex of the germline. The imprinted genes regulate and interact with other genes, consistent with the existence of an imprinted gene network. Defects of genomic imprinting result in syndromal imprinting disorders. To date a dozen congenital imprinting disorders are known. Usually, a given imprinting disorder can be caused by different types of defects, including point mutations, deletions/duplications, uniparental disomy, and epimutations. Causative trans-acting factors in imprinting disorders, including ZFP57 and the subcortical maternal complex (SCMC), have the potential to affect multiple DMRs across the genome, resulting in a multi-locus imprinting disturbance. There is evidence that mutations in components of the SCMC can confer an increased risk for imprinting disorders.
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Stephenson, Jessica F., and Michael Reynolds. "Imprinting can cause a maladaptive preference for infectious conspecifics." Biology Letters 12, no. 4 (April 2016): 20160020. http://dx.doi.org/10.1098/rsbl.2016.0020.
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Recognizing and associating with specific individuals, such as conspecifics or kin, brings many benefits. One mechanism underlying such recognition is imprinting: the long-term memory of cues encountered during development. Typically, juveniles imprint on cues of nearby individuals and may later associate with phenotypes matching their ‘recognition template’. However, phenotype matching could lead to maladaptive social decisions if, for instance, individuals imprint on the cues of conspecifics infected with directly transmitted diseases. To investigate the role of imprinting in the sensory ecology of disease transmission, we exposed juvenile guppies, Poecilia reticulata , to the cues of healthy conspecifics, or to those experiencing disease caused by the directly transmitted parasite Gyrodactylus turnbulli . In a dichotomous choice test, adult ‘disease-imprinted’ guppies preferred to associate with the chemical cues of G. turnbulli -infected conspecifics, whereas ‘healthy-imprinted’ guppies preferred to associate with cues of uninfected conspecifics. These responses were only observed when stimulus fish were in late infection, suggesting imprinted fish responded to cues of disease, but not of infection alone. We discuss how maladaptive imprinting may promote disease transmission in natural populations of a social host.
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Mikhak, Zamaneh, James P. Strassner, and Andrew D. Luster. "Lung dendritic cells imprint T cell lung homing and promote lung immunity through the chemokine receptor CCR4." Journal of Experimental Medicine 210, no. 9 (August 19, 2013): 1855–69. http://dx.doi.org/10.1084/jem.20130091.
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T cell trafficking into the lung is critical for lung immunity, but the mechanisms that mediate T cell lung homing are not well understood. Here, we show that lung dendritic cells (DCs) imprint T cell lung homing, as lung DC–activated T cells traffic more efficiently into the lung in response to inhaled antigen and at homeostasis compared with T cells activated by DCs from other tissues. Consequently, lung DC–imprinted T cells protect against influenza more effectively than do gut and skin DC–imprinted T cells. Lung DCs imprint the expression of CCR4 on T cells, and CCR4 contributes to T cell lung imprinting. Lung DC–activated, CCR4-deficient T cells fail to traffic into the lung as efficiently and to protect against influenza as effectively as lung DC–activated, CCR4-sufficient T cells. Thus, lung DCs imprint T cell lung homing and promote lung immunity in part through CCR4.
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Mangia, Anita, Annalisa Chiriatti, Patrizia Chiarappa, Maria Angela Incalza, Giovanni Antonaci, Brunella Pilato, Giovanni Simone, Stefania Tommasi, and Angelo Paradiso. "Touch Imprint Cytology in Tumor Tissue Banks for the Confirmation of Neoplastic Cellularity and for DNA Extraction." Archives of Pathology & Laboratory Medicine 132, no. 6 (June 1, 2008): 974–78. http://dx.doi.org/10.5858/2008-132-974-ticitt.
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Abstract Context.—Learning the characteristics of frozen tissue samples stored in tumor banks for biological studies remains a problem. Objective.—To assess the use of touch imprint cytology on fresh tissue samples as a rapid and reliable method of determining the presence and quantity of neoplastic cells before freezing. Design.—Touch imprint cytology was performed on 259 specimens of operable breast cancer. Touch imprints were prepared from fresh tissue specimens before freezing samples for storage. Each tumor sample was imprinted on a glass slide and stained with hematoxylin-eosin. Tumor cellularity was quantified as negative, poor, moderate, or rich. Results.—A significant correlation was found between samples with a tumor size greater than 2 cm and high tumor cellularity (P = .03; χ2 test). Furthermore, 35% of ductal tumors showed higher tumor cellularity compared with lobular tumors (P < .001; χ2 test). No association was found between lymph node status and tumor grade. When samples for which more than 2 imprints were available were examined, tumor cellularity among imprints of the same sample showed an overall agreement of 0.67 (P < .001; κ statistic). It was also determined that the higher the cellularity, the higher the agreement. Our data also showed concordance of 0.87 (P < .001; κ statistic) between touch imprint cytology imprints and histologic sections from contiguous tumor. Moreover, 11 randomly selected samples underwent DNA extraction, polymerase chain reaction, and sequencing to verify the feasibility of DNA analyses. We found that DNA from touch imprint cytology was amplifiable and suitable for direct sequencing. Conclusions.—Touch imprint cytology may represent an important step in the quality control of tumor cellularity of breast cancer specimens designed to be stored in tumor biobanks and a valid method for assessing the suitability of such tissue for further biomorphologic and biomolecular applications.
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Lee, Jiyoung, Kimiko Inoue, Ryuichi Ono, Narumi Ogonuki, Takashi Kohda, Tomoko Kaneko-Ishino, Atsuo Ogura, and Fumitoshi Ishino. "Erasing genomic imprinting memory in mouse clone embryos produced from day 11.5 primordial germ cells." Development 129, no. 8 (April 15, 2002): 1807–17. http://dx.doi.org/10.1242/dev.129.8.1807.
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Genomic imprinting is an epigenetic mechanism that causes functional differences between paternal and maternal genomes, and plays an essential role in mammalian development. Stage-specific changes in the DNA methylation patterns of imprinted genes suggest that their imprints are erased some time during the primordial germ cell (PGC) stage, before their gametic patterns are re-established during gametogenesis according to the sex of individuals. To define the exact timing and pattern of the erasure process, we have analyzed parental-origin-specific expression of imprinted genes and DNA methylation patterns of differentially methylated regions (DMRs) in embryos, each derived from a single day 11.5 to day 13.5 PGC by nuclear transfer. Cloned embryos produced from day 12.5 to day 13.5 PGCs showed growth retardation and early embryonic lethality around day 9.5. Imprinted genes lost their parental-origin-specific expression patterns completely and became biallelic or silenced. We confirmed that clones derived from both male and female PGCs gave the same result, demonstrating the existence of a common default state of genomic imprinting to male and female germlines. When we produced clone embryos from day 11.5 PGCs, their development was significantly improved, allowing them to survive until at least the day 11.5 embryonic stage. Interestingly, several intermediate states of genomic imprinting between somatic cell states and the default states were seen in these embryos. Loss of the monoallelic expression of imprinted genes proceeded in a step-wise manner coordinated specifically for each imprinted gene. DNA demethylation of the DMRs of the imprinted genes in exact accordance with the loss of their imprinted monoallelic expression was also observed. Analysis of DNA methylation in day 10.5 to day 12.5 PGCs demonstrated that PGC clones represented the DNA methylation status of donor PGCs well. These findings provide strong evidence that the erasure process of genomic imprinting memory proceeds in the day 10.5 to day 11.5 PGCs, with the timing precisely controlled for each imprinted gene. The nuclear transfer technique enabled us to analyze the imprinting status of each PGC and clearly demonstrated a close relationship between expression and DNA methylation patterns and the ability of imprinted genes to support development.
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Yu, Chen-Chieh, Yi-Chuan Tseng, Pao-Yun Su, Keng-Te Lin, Chang-Ching Shao, Sin-Yi Chou, Yu-Ting Yen, and Hsuen-Li Chen. "Incident angle–tuned, broadband, ultrahigh-sensitivity plasmonic antennas prepared from nanoparticles on imprinted mirrors." Nanoscale 7, no. 9 (2015): 3985–96. http://dx.doi.org/10.1039/c4nr05902f.
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We have used a direct imprint-in-metal method that is cheap and rapid to prepare incident angle-tuned, broadband, ultrahigh-sensitivity plasmonic antennas from nanoparticles (NPs) and imprinted metal mirrors.
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Zhuang, Hai Yan, Hui Zhi Li, and Yang Xue. "Synthesis, Characterization and Selective Recognition of Lead Using a New Ion Imprinted Polymer Material." Advanced Materials Research 306-307 (August 2011): 688–91. http://dx.doi.org/10.4028/www.scientific.net/amr.306-307.688.
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A new ion-imprinted polymer (IIP) material was synthesized by copolymerization of 4-vinylpyridine(VP) as monomer, ethylene glycol dimethacrylate(EGDMA) as crosslinking agent and 2,2΄-azobisisobutyronitrile(AIBN) as initiator in the presence of Pb–1,5-diphenylcarbazone(Pb-DHCB) complex. Blank non-imprinted polymer (NIP) were prepared under identical conditions without the use of lead imprint ion. The synthesized polymers were characterized by IR spectroscopy and elemental analyzer techniques. Of the several polymers synthesized, only the imprinted polymer formed with binary complex of Pb2+–DHCB showed quantitative enrichment of lead ion from aqueous solution. The relative standard deviation of the five replicate determinations of Pb (II) was3.26%. The detection limit for 150 mL of sample was 1.6 µg L-1 using flame atomic absorption spectrometry. The developed method was successfully applied to the determination of trace lead in environmental samples with satisfactory results.
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Zheng, Xiaofeng, Sohayb Khaoulani, Nadia Ktari, Momath Lo, Ahmed M. Khalil, Chouki Zerrouki, Najla Fourati, and Mohamed M. Chehimi. "Towards Clean and Safe Water: A Review on the Emerging Role of Imprinted Polymer-Based Electrochemical Sensors." Sensors 21, no. 13 (June 23, 2021): 4300. http://dx.doi.org/10.3390/s21134300.
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This review critically summarizes the knowledge of imprinted polymer-based electrochemical sensors for the detection of pesticides, metal ions and waterborne pathogenic bacteria, focusing on the last five years. MIP-based electrochemical sensors exhibit low limits of detection (LOD), high selectivity, high sensitivity and low cost. We put the emphasis on the design of imprinted polymers and their composites and coatings by radical polymerization, oxidative polymerization of conjugated monomers or sol-gel chemistry. Whilst most imprinted polymers are used in conjunction with differential pulse or square wave voltammetry for sensing organics and metal ions, electrochemical impedance spectroscopy (EIS) appears as the chief technique for detecting bacteria or their corresponding proteins. Interestingly, bacteria could also be probed via their quorum sensing signaling molecules or flagella proteins. If much has been developed in the past decade with glassy carbon or gold electrodes, it is clear that carbon paste electrodes of imprinted polymers are more and more investigated due to their versatility. Shortlisted case studies were critically reviewed and discussed; clearly, a plethora of tricky strategies of designing selective electrochemical sensors are offered to “Imprinters”. We anticipate that this review will be of interest to experts and newcomers in the field who are paying time and effort combining electrochemical sensors with MIP technology.
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Fan, X. Q., H. H. Zhang, S. Liu, K. Jia, and Z. Y. Gan. "Fabrication of Nanoscale Gratings by Nanoimprint on Silicon Wafer." Key Engineering Materials 315-316 (July 2006): 825–28. http://dx.doi.org/10.4028/www.scientific.net/kem.315-316.825.
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This paper presents an approach to fabricate nanoscale gratings by direct imprint on silicon substrate. Imprint conditions that affect the transcription accuracy, such as imprint temperature and pressure, are discussed, and the profile of the imprinted 80nm width gratings with a 250 nm pitch is checked by SEM. High fidelity and fine uniformity demonstrate that nanoimprint is an economical and efficient method to fabricate nanoscale gratings.
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Hata, Kenichiro, Masaki Okano, Hong Lei, and En Li. "Dnmt3L cooperates with the Dnmt3 family of de novo DNA methyltransferases to establish maternal imprints in mice." Development 129, no. 8 (April 15, 2002): 1983–93. http://dx.doi.org/10.1242/dev.129.8.1983.
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Genomic imprinting is regulated by differential methylation of the paternal and maternal genome. However, it remains unknown how parental imprinting is established during gametogenesis. In this study, we demonstrate that Dnmt3L, a protein sharing homology with DNA methyltransferases, Dnmt3a and Dnmt3b, but lacking enzymatic activity, is essential for the establishment of maternal methylation imprints and appropriate expression of maternally imprinted genes. We also show that Dnmt3L interacts with Dnmt3a and Dnmt3b and co-localizes with these enzymes in the nuclei of transfected cells, suggesting that Dnmt3L may regulate genomic imprinting via the Dnmt3 family enzymes. Consistent with this model, we show that [Dnmt3a–/–, Dnmt3b+/–] mice also fail to establish maternal methylation imprints. In addition, both Dnmt3a and Dnmt3L are required for spermatogenesis. Together, our findings suggest that Dnmt3L may cooperate with Dnmt3 family methyltransferases to carry out de novo methylation of maternally imprinted genes in oocytes.
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Liu, Qing Peng, Hui Zhi Li, Hai Yan Zhuang, and Mei Shan Pei. "Synthesis of a New Ion Imprinted Polymer Material for Separation and Preconcentration of Traces of Neodymium Ions." Advanced Materials Research 306-307 (August 2011): 705–8. http://dx.doi.org/10.4028/www.scientific.net/amr.306-307.705.
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Neodymium ion imprinted polymers (IIP) were synthesized by formation of ternary complexes of neodymium ion with Vanillin Benzidine(VLB) and 4-vinylpyridine (VP) as chelating agent following copolymerizing with styrene as functional monomer and ethylene glycol dimethacrylate (EGDMA) as cross-linking monomer using 2,2´-azobisisobutyronitrile as initiator. Control polymers（CPs） were prepared under identical conditions without the use of neodymium imprint ion. The synthesized polymers were characterized by IR spectroscopy and elemental analyzer techniques. Of the several polymers synthesized, only the imprinted polymer formed with ternary complex of Nd3+–VLB–VP(1:1:2 IIP) showed quantitative enrichment of neodymium ion from aqueous solution.
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Reik, Wolf, Fatima Santos, Kohzoh Mitsuya, Hugh Morgan, and Wendy Dean. "Epigenetic asymmetry in the mammalian zygote and early embryo: relationship to lineage commitment?" Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 358, no. 1436 (August 29, 2003): 1403–9. http://dx.doi.org/10.1098/rstb.2003.1326.
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Epigenetic asymmetry between parental genomes and embryonic lineages exists at the earliest stages of mammalian development. The maternal genome in the zygote is highly methylated in both its DNA and its histones and most imprinted genes have maternal germline methylation imprints. The paternal genome is rapidly remodelled with protamine removal, addition of acetylated histones, and rapid demethylation of DNA before replication. A minority of imprinted genes have paternal germline methylation imprints. Methylation and chromatin reprogramming continues during cleavage divisions, but at the blastocyst stage lineage commitment to inner cell mass (ICM) or trophectoderm (TE) fate is accompanied by a dramatic increase in DNA and histone methylation, predominantly in the ICM. This may set up major epigenetic differences between embryonic and extraembryonic tissues, including in X–chromosome inactivation and perhaps imprinting. Maintaining epigenetic asymmetry appears important for development as asymmetry is lost in cloned embryos, most of which have developmental defects, and in particular an imbalance between extraembryonic and embryonic tissue development.
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Monk, David, Philippe Arnaud, Jennifer M. Frost, Andrew J. Wood, Michael Cowley, Alejandro Martin-Trujillo, Amy Guillaumet-Adkins, et al. "Human imprinted retrogenes exhibit non-canonical imprint chromatin signatures and reside in non-imprinted host genes." Nucleic Acids Research 39, no. 11 (February 7, 2011): 4577–86. http://dx.doi.org/10.1093/nar/gkq1230.
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Mackin, Sarah-Jayne, Avinash Thakur, and Colum P. Walsh. "Imprint stability and plasticity during development." Reproduction 156, no. 2 (August 2018): R43—R55. http://dx.doi.org/10.1530/rep-18-0051.
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There have been a number of recent insights in the area of genomic imprinting, the phenomenon whereby one of two autosomal alleles is selected for expression based on the parent of origin. This is due in part to a proliferation of new techniques for interrogating the genome that are leading researchers working on organisms other than mouse and human, where imprinting has been most studied, to become interested in looking for potential imprinting effects. Here, we recap what is known about the importance of imprints for growth and body size, as well as the main types of locus control. Interestingly, work from a number of labs has now shown that maintenance of the imprint post implantation appears to be a more crucial step than previously appreciated. We ask whether imprints can be reprogrammed somatically, how many loci there are and how conserved imprinted regions are in other species. Finally, we survey some of the methods available for examining DNA methylation genome-wide and look to the future of this burgeoning field.
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Rodrigues, Jessica A., Ping-Hung Hsieh, Deling Ruan, Toshiro Nishimura, Manoj K. Sharma, Rita Sharma, XinYi Ye, et al. "Divergence among rice cultivars reveals roles for transposition and epimutation in ongoing evolution of genomic imprinting." Proceedings of the National Academy of Sciences 118, no. 29 (July 16, 2021): e2104445118. http://dx.doi.org/10.1073/pnas.2104445118.
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Parent-of-origin–dependent gene expression in mammals and flowering plants results from differing chromatin imprints (genomic imprinting) between maternally and paternally inherited alleles. Imprinted gene expression in the endosperm of seeds is associated with localized hypomethylation of maternally but not paternally inherited DNA, with certain small RNAs also displaying parent-of-origin–specific expression. To understand the evolution of imprinting mechanisms in Oryza sativa (rice), we analyzed imprinting divergence among four cultivars that span both japonica and indica subspecies: Nipponbare, Kitaake, 93-11, and IR64. Most imprinted genes are imprinted across cultivars and enriched for functions in chromatin and transcriptional regulation, development, and signaling. However, 4 to 11% of imprinted genes display divergent imprinting. Analyses of DNA methylation and small RNAs revealed that endosperm-specific 24-nt small RNA–producing loci show weak RNA-directed DNA methylation, frequently overlap genes, and are imprinted four times more often than genes. However, imprinting divergence most often correlated with local DNA methylation epimutations (9 of 17 assessable loci), which were largely stable within subspecies. Small insertion/deletion events and transposable element insertions accompanied 4 of the 9 locally epimutated loci and associated with imprinting divergence at another 4 of the remaining 8 loci. Correlating epigenetic and genetic variation occurred at key regulatory regions—the promoter and transcription start site of maternally biased genes, and the promoter and gene body of paternally biased genes. Our results reinforce models for the role of maternal-specific DNA hypomethylation in imprinting of both maternally and paternally biased genes, and highlight the role of transposition and epimutation in rice imprinting evolution.
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Chakraborty, Soma, and Xyza Jane Templonuevo. "Removal of Triolein Lipid From Aqueous System by Molecularly Imprinted Chitosan and Its Derivative." KIMIKA 29, no. 1 (May 18, 2018): 11–16. http://dx.doi.org/10.26534/kimika.v29i1.11-16.
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Chitosan was molecularly imprinted to remove triolein (a model lipid triacylglyceride) from water. Molecularly-imprinted chitosan (chitosan-MIP) was synthesized by crosslinking it with glutaraldehyde in the presence of triolein as the template at 50°C for 2h. MIPs of octanoyl derivative of chitosan(Oct-MIP) were also prepared by similar method. Octanoyl chitosan was synthesized by N-acylation of chitosan using octanoyl chloride at room temperature for 12h. Contact angle measurements of water droplet on chitosan and octanoyl chitosan revealed increased hydrophobicity of octanoyl derivative of chitosan. FTIR spectroscopy was used to characterize the derivative and the MIPs. All the synthesized polymers. Oct-MIP and chitosan-MIP could imprint approximately 77% and 66% of triolein template, respectively. Binding experiments revealed that Oct-MIP exhibit higher triolein binding capacity than corresponding non-acylated polymers. In 6h, 1mg of Oct-MIP and chitosan-MIP could rebind 534.50µg and 380.35µg of triolein respectively. Non Imprinted octanoyl chitosan and chitosan bound 272µg and 198.24µg triolein respectively. Both types of MIPs could also bind a triolein analog (1,3-dioleoyl-2-palmitoyl glycerol).
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Xu, Zhi Gang, Zhi Min Liu, and Yun Li Chen. "Mixed-Template Molecularly Imprinted Technique and its Application Research." Advanced Materials Research 787 (September 2013): 99–105. http://dx.doi.org/10.4028/www.scientific.net/amr.787.99.
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Molecularly imprinted techniques have been rapidly developed in recent decade. Some novel molecularly imprinted techniques and some novel application forms of molecularly imprinted polymers have been developed. And it has been widely used in sample pretreatment. In this paper, novel mixed-template molecularly imprinted techniques are introduced. The development and applications of mixed-template molecularly imprinted techniques in recent decade are reviewed, including dual-template molecularly imprinted technique and multi-template molecularly imprinted technique, and its application in chromatographic solid phase, solid phase extraction and microsphere extraction. Moreover, the trends of mixed-template molecularly imprinted techniques in sample pretreatment are prospected.
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Xu, Zhi Gang. "Molecularly Imprinted Polymers for the Analysis of Environmental Estrogen Bisphenol A." Advanced Materials Research 894 (February 2014): 143–48. http://dx.doi.org/10.4028/www.scientific.net/amr.894.143.
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Molecularly imprinted polymer (MIP) has the characteristics of predetermination, specific recognition and practicability. It can eliminate the interference of complicated matrix. It has been widely used as selective adsorption material in sample preparation. Bisphenol A is a common endocrine disruptor in environment. Its toxic effects and analysis have attracted widespread concern. In this paper, the molecularly imprinted sample preparation techniques for bisphenol A were comprehensively reported, including molecularly imprinted microspheres extraction, molecularly imprinted solid phase extraction, molecularly imprinted solid phase microextraction, molecularly imprinted stir bar sorptive extraction and molecularly imprinted membrane extraction. Moreover, the trends of BPA-molecularly imprinted techniques are prospected.
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Horii, T., M. Kimura, S. Morita, Y. Nagao, and I. Hatada. "222 LOSS OF IMPRINTS OF PARTHENOGENETIC EMBRYONIC STEM CELLS IN MURINE CHIMERAS." Reproduction, Fertility and Development 19, no. 1 (2007): 228. http://dx.doi.org/10.1071/rdv19n1ab222.
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Mammalian parthenotes with the 2 maternal genomes cannot develop to term. By contrast, chimeras produced by parthenogenetic and normal embryos can develop to term. However, parthenogenetic cells contribute to restricted cells and body weights of the chimeras are reduced. These effects are due to aberrant expressions of imprinted genes, with complete methylation of the maternally methylated genes and complete loss of the paternally methylated genes. On the other hand, parthenogenetic ES (PGES) chimeras show more normal tissue contribution of donor cells and body weight compared to parthenogenetic embryo (PG) chimeras. To elucidate the epigenetic mechanisms underlying this, we analyzed the epigenetic status of maternally methylated genes in murine PG and PGES chimeras. To make parthenogenetic chimeras, PG and PGES cells which express green fluorescent protein (GFP) were introduced into normal host embryos. Mouse embryonic fibroblasts (MEFs) from E13.5 chimeric fetuses were sorted by the fluorescence-activated cell sorter (FACS). Methylation status of parthenogenetic cells was analyzed by combined bisulfite restriction analysis (COBRA) and bisulfite sequencing. Methylation of maternally methylated genes, Peg1/Mest, Snrpn, and Igf 2r, was almost totally maintained in PG chimeras. Average methylatation percentages of PG-derived MEFs were 80% in Peg1/Mest, 84% in Snrpn, and 81% in Igf 2r (n = 6). In contrast, methylation in some PGES chimeras was partially reduced to normal level in all 3 genes (10–45%, n = 7). To clarify whether demethylation is correlated with expression of the imprinted genes, gene expression was analyzed by quantitative real-time RT-PCR. Among maternally imprinted genes, Peg1/Mest and Snrpn are expressed from the paternal allele, whereas Igf 2r is expressed from the maternal allele. Therefore, in parthenogenetic cells, loss of imprints is expected to up-regulate Peg1/Mest and Snrpn expression, and down-regulate Igf 2r expression. In fact, PGES-derived MEFs were up-regulated in Peg1/Mest and Snrpn expression, and down-regulated in Igf 2r expression. This study revealed that variations of imprint status were observed frequently in somatic cells of PGES cell origin. Demethylation could have occurred during establishment and/or maintenance of PGES cells. This demethylation that occurred in PGES cells could reprogram the maternally methylated imprinted genes and improve tissue contribution and body weight to normal level. The PGES cells with reprogramming ability might be utilized for fertility treatment and regenerative medicine.
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Szabó, Piroska E., Gerd P. Pfeifer, and Jeffrey R. Mann. "Characterization of Novel Parent-Specific Epigenetic Modifications Upstream of the Imprinted Mouse H19Gene." Molecular and Cellular Biology 18, no. 11 (November 1, 1998): 6767–76. http://dx.doi.org/10.1128/mcb.18.11.6767.
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ABSTRACT Genomic imprinting results in parent-specific monoallelic expression of a small number of genes in mammals. The identity of imprints is unknown, but much evidence points to a role for DNA methylation. The maternal alleles of the imprinted H19 gene are active and hypomethylated; the paternal alleles are inactive and hypermethylated. Roles for other epigenetic modifications are suggested by allele-specific differences in nuclease hypersensitivity at particular sites. To further analyze the possible epigenetic mechanisms determining monoallelic expression of H19, we have conducted in vivo dimethylsulfate and DNase I footprinting of regions upstream of the coding sequence in parthenogenetic and androgenetic embryonic stem cells. These cells carry only maternally and paternally derived alleles, respectively. We observed the presence of maternal-allele-specific dimethylsulfate and DNase I footprints at the promoter indicative of protein-DNA interactions at a CCAAT box and at binding sites for transcription factors Sp1 and AP-2. Also, at the boundary of a region further upstream for which existent differential methylation has been suggested to constitute an imprint, we observed a number of strand-specific dimethylsulfate reactivity differences specific to the maternal allele, along with an unusual chromatin structure in that both strands of maternally derived DNA were strongly hypersensitive to DNase I cutting over a distance of 100 nucleotides. We therefore reveal the existence of novel parent-specific epigenetic modifications, which in addition to DNA methylation, could constitute imprints or maintain monoallelic expression of H19.
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Roth, Stephan Volkher, Ralph Döhrmann, Rainer Gehrke, Ralf Röhlsberger, Kai Schlage, Ezzeldin Metwalli, Volker Körstgens, et al. "Mapping the morphological changes of deposited gold nanoparticles across an imprinted groove." Journal of Applied Crystallography 48, no. 6 (November 10, 2015): 1827–33. http://dx.doi.org/10.1107/s1600576715017987.
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The gradient gold layer morphology below the percolation threshold along a channel groove imprinted into a pressure-sensitive adhesive polymer film is studied. In order to elucidate the complex nanostructure of the sputter-deposited gold nanoparticle layer, nanobeam grazing-incidence small-angle X-ray scattering and imaging ellipsometry are used. Thus, the complex nanostructure of this metal–polymer nanocomposite can be detected, distinguished and identified. The presence of macroscopically curved structures, as introduced by the imprinted ridges, can cause deviations from the mean metal nanoparticle morphology, probed on the `flat' sample area outside the ridges. The phase-separated morphology of the polymer film is rather unaffected by the imprint structure but leads, in addition, to a selective growth of gold on polystyrene-rich domains.
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Murrell, Adele, and Santiago Uribe-Lewis. "Genomic imprinting and cancer: Remembering the parental origin." Biochemist 32, no. 5 (October 1, 2010): 26–29. http://dx.doi.org/10.1042/bio03205026.
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Genomic imprinting results in only one copy of a diploid pair of alleles being expressed in a parentof-origin-specific manner. The ‘imprint’ encodes a memory of whether a gene came through the maternal or paternal line and contains the information that decides which parental copy will be active or silent. Imprints are established in the developing gametes, passed on to the next generation after fertilization where they are read and maintained in the somatic cells or erased and reset in the germ cells. The components of the ‘memory’ are a combination of epigenetic features such as DNA methylation, post-translational histone modifications and protein/RNA factors that can bind to DNA and label the genes such that a cell's transcription machinery can distinguish between maternal and paternal alleles. Most imprinted genes are associated with sequences that are methylated on only one parental allele, known as differentially methylated regions (DMRs).
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Anisimov, Sergey V. "A Prevalence of Imprinted Genes within the Total Transcriptomes of Human Tissues and Cells." Molecular Biology International 2012 (September 11, 2012): 1–29. http://dx.doi.org/10.1155/2012/793506.
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Genomic imprinting is an epigenetic phenomenon that causes a differential expression of paternally and maternally inherited alleles of a subset of genes (the so-called imprinted genes). Imprinted genes are distributed throughout the genome and it is predicted that about 1% of the human genes may be imprinted. It is recognized that the allelic expression of imprinted genes varies between tissues and developmental stages. The current study represents the first attempt to estimate a prevalence of imprinted genes within the total human transcriptome. In silico analysis of the normalized expression profiles of a comprehensive panel of 173 established and candidate human imprinted genes was performed, in 492 publicly available SAGE libraries. The latter represent human cell and tissue samples in a variety of physiological and pathological conditions. Variations in the prevalence of imprinted genes within the total transcriptomes (ranging from 0.08% to 4.36%) and expression profiles of the individual imprinted genes are assessed. This paper thus provides a useful reference on the size of the imprinted transcriptome and expression of the individual imprinted genes.
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Renfree, Marilyn B., Eleanor I. Ager, Geoff Shaw, and Andrew J. Pask. "Genomic imprinting in marsupial placentation." REPRODUCTION 136, no. 5 (November 2008): 523–31. http://dx.doi.org/10.1530/rep-08-0264.
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Genomic imprinting is a widespread epigenetic phenomenon in eutherian mammals, which regulates many aspects of growth and development. Parental conflict over the degree of maternal nutrient transfer is the favoured hypothesis for the evolution of imprinting. Marsupials, like eutherian mammals, are viviparous but deliver an altricial young after a short gestation supported by a fully functional placenta, so can shed light on the evolution and time of acquisition of genomic imprinting. All orthologues of eutherian imprinted genes examined have a conserved expression in the marsupial placenta regardless of their imprint status. Differentially methylated regions (DMRs) are the most common mechanism controlling genomic imprinting in eutherian mammals, but none were found in the marsupial imprinted orthologues of IGF2 receptor (IGF2R), INS or mesoderm-specific transcript (MEST). Instead, histone modification appears to be the mechanism used to silence these genes. At least three genes in marsupials have DMRs: H19, IGF2 and PEG10. PEG10 is particularly interesting as it is derived from a retrotransposon, providing the first direct evidence that retrotransposon insertion can drive the evolution of an imprinted region and of a DMR in mammals. The insertion occurred after the prototherian–therian mammal divergence, suggesting that there may have been strong selection for the retention of imprinted regions that arose during the evolution of placentation. There is currently no evidence for genomic imprinting in the egg-laying monotreme mammals. However, since these mammals do have a short-lived placenta, imprinting appears to be correlated with viviparity but not placentation.
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Lin, Chun Xiang, Ming Hua Liu, and Huai Yu Zhan. "Pb(II)-Imprinted Polymer Prepared by Graft Copolymerization of Acrylic Acid onto Cellulose." Advanced Materials Research 295-297 (July 2011): 2045–48. http://dx.doi.org/10.4028/www.scientific.net/amr.295-297.2045.
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The Pb( )-imprinted polymers were synthesized through homogeneous graft copolymerization of cellulose with acrylic acid in an homogeneous medium using Pb( ) as template. The prepared copolymers were characterized by FTIR and SEM. The batch adsorption experiments were conducted to evaluate the adsorption capacity of the Pb( )-imprinted beads. The results demonstrated that the imprinted beads showed significantly higher imprinting efficiency than those only consisting of poly(acrylic acid) without Pb( )-imprinted, and the selectively adsorption capacity of Pb( ) on imprinted beads was higher than other competitive ions(Cu( ) or Ni( )). The imprinted beads also showed much better stability in rebinding of the imprinted ions after three adsorption-regeneration cycles.
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de Koning, Dirk-Jan, Henk Bovenhuis, and Johan A. M. van Arendonk. "On the Detection of Imprinted Quantitative Trait Loci in Experimental Crosses of Outbred Species." Genetics 161, no. 2 (June 1, 2002): 931–38. http://dx.doi.org/10.1093/genetics/161.2.931.
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Abstract In this article, the quantitative genetic aspects of imprinted genes and statistical properties of methods to detect imprinted QTL are studied. Different models to detect imprinted QTL and to distinguish between imprinted and Mendelian QTL were compared in a simulation study. Mendelian and imprinted QTL were simulated in an F2 design and analyzed under Mendelian and imprinting models. Mode of expression was evaluated against the H0 of a Mendelian QTL as well as the H0 of an imprinted QTL. It was shown that imprinted QTL might remain undetected when analyzing the genome with Mendelian models only. Compared to testing against a Mendelian QTL, using the H0 of an imprinted QTL gave a higher proportion of correctly identified imprinted QTL, but also gave a higher proportion of false inference of imprinting for Mendelian QTL. When QTL were segregating in the founder lines, spurious detection of imprinting became more prominent under both tests, especially for designs with a small number of F1 sires.
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Weitzman, Jonathan B. "Imprinted inactivation." Genome Biology 2 (2001): spotlight—20010730–01. http://dx.doi.org/10.1186/gb-spotlight-20010730-01.
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Whitcombe, M. J., and E. N. Vulfson. "Imprinted Polymers." Advanced Materials 13, no. 7 (April 2001): 467–78. http://dx.doi.org/10.1002/1521-4095(200104)13:7<467::aid-adma467>3.0.co;2-t.
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Mujahid, Adnan, Faisal Amin, Tajamal Hussain, Naseer Iqbal, Asma Tufail Shah, and Adeel Afzal. "Synthesis of Imprinted Polysiloxanes for Immobilization of Metal ions." MRS Proceedings 1675 (2014): 209–14. http://dx.doi.org/10.1557/opl.2014.867.
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ABSTRACTImprinting is a well-established technique to induce recognition features in both organic and inorganic materials for a variety of target analytes. In this study, ion imprinted polysiloxanes with varying percentage of coupling agent i.e. 3-chloro propyl trimethoxy silane (CPTM) were synthesized by sol-gel method for imprinting of Cr3+. The imprinting of Cr3+ in cross-linked siloxane network was investigated by FT-IR which indicates the metal ion is coordinated with oxygen atoms of polysiloxanes. SEM images revealed that imprinted polysiloxanes possess uniform particles of submicron size. It was experienced that by increasing the concentration of CPTM up to 10% (v/v) substantially improves the binding capacity of polysiloxanes which allows us to recognized Cr3+ down to 50µg/L. Furthermore, the selectivity of Cr3+-imprinted polysiloxanes was evaluated by treating them with other competing metal ions of same concentration i.e. Cr6+, Pb2+ and Ni2+. In this regard, polysiloxanes showed much higher binding for imprint ion i.e. Cr3+ in comparison to above mentioned metal ions. Finally, the regenerated polysiloxanes were studied in order to reuse them thus, developing cost effective biomimetic sensor coatings.
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Fahey, Marie E., Walter Mills, Desmond G. Higgins, and Tom Moore. "Maternally and Paternally Silenced Imprinted Genes Differ in Their Intron Content." Comparative and Functional Genomics 5, no. 8 (2004): 572–83. http://dx.doi.org/10.1002/cfg.437.
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Imprinted genes exhibit silencing of one of the parental alleles during embryonic development. In a previous study imprinted genes were found to have reduced intron content relative to a non-imprinted control set (Hurstet al., 1996). However, due to the small sample size, it was not possible to analyse the source of this effect. Here, we re-investigate this observation using larger datasets of imprinted and control (non-imprinted) genes that allow us to consider mouse and human, and maternally and paternally silenced, imprinted genes separately. We find that, in the human and mouse, there is reduced intron content in the maternally silenced imprinted genes relative to a non-imprinted control set. Among imprinted genes, a strong bias is also observed in the distribution of intronless genes, which are found exclusively in the maternally silenced dataset. The paternally silenced dataset in the human is not different to the control set; however, the mouse paternally silenced dataset has more introns than the control group. A direct comparison of mouse maternally and paternally silenced imprinted gene datasets shows that they differ significantly with respect to a variety of intron-related parameters. We discuss a variety of possible explanations for our observations.
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Mi, Zhi Yuan, Zhuo Ma, Xiao Li Li, Wei De Xiong, and Ying Qing Zhang. "Recognition of Papain by Konjac Glucomannan-Based Molecularly Imprinted Membrane." Advanced Materials Research 282-283 (July 2011): 687–90. http://dx.doi.org/10.4028/www.scientific.net/amr.282-283.687.
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Objective: To prepare a novel protein molecularly imprinted membrane. Methods: Konjac glucomanan was swollen, cross-linked, added papain and glycerol, dried to form imprinted membranes. Results: After eluted, the rebinding adsorption amounts of papain for imprinted and blank membranes were (12.692±3.452) μg/cm2 and (7.849±2.321) μg/cm2 respectively. The papain imprinted membrane had the highest imprinted factor α 1.8 for papain than for other proteins. Results of FT-IR and SEM showed that the cavity structure of the eluted membrane provided space for rebinding. Conclusions: Konjac glucomannan-based imprinted membrane has good specific adsorption and selective recognition abilities for the templates- papain, and shows great possibilities to be a promising protein molecularly imprinted polymer.
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Saferali, Aabida, Sanny Moussette, Donovan Chan, Jacquetta Trasler, Taiping Chen, Rima Rozen, and Anna K. Naumova. "DNA methyltransferase 1 (Dnmt1) mutation affects Snrpn imprinting in the mouse male germ line." Genome 55, no. 09 (September 2012): 673–82. http://dx.doi.org/10.1139/g2012-056.
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DNA methylation and DNA methyltransferases are essential for spermatogenesis. Mutations in the DNA methyltransferase Dnmt1 gene exert a paternal effect on epigenetic states and phenotypes of offspring, suggesting that DNMT1 is important for the epigenetic remodeling of the genome that takes place during spermatogenesis. However, the specific role of DNMT1 in spermatogenesis and the establishment of genomic imprints in the male germ line remains elusive. To further characterize the effect of DNMT1 deficiency on the resetting of methylation imprints during spermatogenesis, we analyzed the methylation profiles of imprinted regions in the spermatozoa of mice that were heterozygous for a Dnmt1 loss-of-function mutation. The mutation did not affect the H19 or IG differentially methylated regions (DMRs) that are usually highly methylated but led to a partial hypermethylation of the Snrpn DMR, a region that should normally be unmethylated in mature spermatozoa. This defect does not appear in mouse models with mutations in Dnmt3a and Mthfr genes and, therefore, it is specific for the Dnmt1 gene and is suggestive of a role of DNMT1 in imprint resetting or maintenance in the male germ line.
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Saylan, Yeşeren, Semra Akgönüllü, Handan Yavuz, Serhat Ünal, and Adil Denizli. "Molecularly Imprinted Polymer Based Sensors for Medical Applications." Sensors 19, no. 6 (March 13, 2019): 1279. http://dx.doi.org/10.3390/s19061279.
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Sensors have been extensively used owing to multiple advantages, including exceptional sensing performance, user-friendly operation, fast response, high sensitivity and specificity, portability, and real-time analysis. In recent years, efforts in sensor realm have expanded promptly, and it has already presented a broad range of applications in the fields of medical, pharmaceutical and environmental applications, food safety, and homeland security. In particular, molecularly imprinted polymer based sensors have created a fascinating horizon for surface modification techniques by forming specific recognition cavities for template molecules in the polymeric matrix. This method ensures a broad range of versatility to imprint a variety of biomolecules with different size, three dimensional structure, physical and chemical features. In contrast to complex and time-consuming laboratory surface modification methods, molecular imprinting offers a rapid, sensitive, inexpensive, easy-to-use, and highly selective approaches for sensing, and especially for the applications of diagnosis, screening, and theranostics. Due to its physical and chemical robustness, high stability, low-cost, and reusability features, molecularly imprinted polymer based sensors have become very attractive modalities for such applications with a sensitivity of minute structural changes in the structure of biomolecules. This review aims at discussing the principle of molecular imprinting method, the integration of molecularly imprinted polymers with sensing tools, the recent advances and strategies in molecular imprinting methodologies, their applications in medical, and future outlook on this concept.