Relevant bibliographies by topics / Mice embryology; mice genetics

Academic literature on the topic 'Mice embryology; mice genetics'

Author: Grafiati
Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Mice embryology; mice genetics"

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Juriloff, D. M., T. M. Gunn, M. J. Harris, D. G. Mah, M. K. Wu, and S. L. Dewell. "Multifactorial genetics of exencephaly in SELH/Bc mice." Teratology 64, no. 4 (2001): 189–200. http://dx.doi.org/10.1002/tera.1064.

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Gabriel, George C., Hisato Yagi, Xinxiu Xu, and Cecilia W. Lo. "Novel Insights into the Etiology, Genetics, and Embryology of Hypoplastic Left Heart Syndrome." World Journal for Pediatric and Congenital Heart Surgery 13, no. 5 (September 2022): 565–70. http://dx.doi.org/10.1177/21501351221102961.

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Hypoplastic left heart syndrome (HLHS) is a relatively rare severe congenital heart defect (CHD) closely linked to other left ventricular outflow tract (LVOT) lesions including bicuspid aortic valve (BAV), one of the most common heart defects. While HLHS, BAV, and other LVOT lesions have a strong genetic underpinning, their genetic etiology remains poorly understood. Findings from a large-scale mouse mutagenesis screen showed HLHS has a multigenic etiology and is genetically heterogenous, explaining difficulties in identifying the genetic causes of HLHS. In Ohia mice, HLHS shows incomplete penetrance. Some mice exhibited small LV with normal aorta, and others a normal LV with hypoplastic aorta, indicating the LV hypoplasia is not hemodynamically driven. In Ohia mutants, HLHS was found to have a digenic modular construction, with mutation in a chromatin modifier causing the small LV phenotype and mutation in Pcdha9 causing the aorta/aortic valve hypoplasia. The Pcdha9 mutation alone can cause BAV, and in the human genome two common deletion copy number variants spanning PCDHA7-10 are associated with BAV. Hence the digenic etiology of HLHS can account for the close association of HLHS, a rare CHD, with BAV, one of the most common CHD. Functional analysis of Ohia HLHS heart tissue showed severe mitochondrial dysfunction in the small LV, while the normal size RV is also affected but milder, suggesting possible role in vulnerability of surgically palliated HLHS patients to heart failure. These findings suggest insights into the genetics of HLHS may yield new therapies for improving outcome for patients with HLHS.
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Naruse, Ichiro, and Yoshiro Kameyama. "Fetal laser surgery in genetic Polydactyly mice." Teratology 41, no. 6 (June 1990): 731–35. http://dx.doi.org/10.1002/tera.1420410610.

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Ruetten, Hannah, Kyle A. Wegner, Helen L. Zhang, Peiqing Wang, Jaskiran Sandhu, Simran Sandhu, Jacquelyn Morkrid, et al. "Insight and Resources From a Study of the “Impact of Sex, Androgens, and Prostate Size on C57BL/6J Mouse Urinary Physiology." Toxicologic Pathology 47, no. 8 (October 29, 2019): 1038–42. http://dx.doi.org/10.1177/0192623319877867.

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The purpose of this symposium report is to summarize information from a session 3 oral presentation at the Society of Toxicologic Pathology Annual Symposium in Raleigh, North Carolina. Mice are genetically tractable and are likely to play an important role in elucidating environmental, genetic, and aging-related mechanisms of urinary dysfunction in men. We and others have made significant strides in developing quantitative methods for assessing mouse urinary function and our collaborators recently showed that aging male mice, like men, develop urinary dysfunction. Yet, it remains unclear how mouse prostate anatomy and histology relate to urinary function. The purpose of this report is to share foundational resources for evaluating mouse prostate histology and urinary physiology from our recent publication “Impact of Sex, Androgens, and Prostate Size on C57BL/6J Mouse Urinary Physiology: Functional Assessment.” We will begin with a review of prostatic embryology in men and mice, then move to comparative histology resources, and conclude with quantitative measures of rodent urinary physiology.
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Mei, Hua, Cara Walters, Richard Carter, and William H. Colledge. "Gpr54−/− mice show more pronounced defects in spermatogenesis than Kiss1−/− mice and improved spermatogenesis with age when exposed to dietary phytoestrogens." REPRODUCTION 141, no. 3 (March 2011): 357–66. http://dx.doi.org/10.1530/rep-10-0432.

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Mice with mutations in the kisspeptin signaling pathway (Kiss1−/− or Gpr54−/−) have low gonadotrophic hormone levels, small testes, and impaired spermatogenesis. Between 2 and 7 months of age, however, the testes of the mutant mice increase in weight and in Gpr54−/− mice, the number of seminiferous tubules containing spermatids/spermatozoa increases from 17 to 78%. In contrast, the Kiss1−/− mice have a less severe defect in spermatogenesis and larger testes than Gpr54−/− mice at both 2 and 7 months of age. The reason for the improved spermatogenesis was investigated. Plasma testosterone and FSH levels did not increase with age in the mutant mice and remained much lower than in wild-type (WT) mice. In contrast, intratesticular testosterone levels were similar between mutant and WT mice. These data indicate that age-related spermatogenesis can be completed under conditions of low plasma testosterone and FSH and that intratesticular testosterone may contribute to this process. In addition, however, when the Gpr54−/− mice were fed a phytoestrogen-free diet, they showed no age-related increase in testes weight or improved spermatogenesis. Thus, both genetic and environmental factors are involved in the improved spermatogenesis in the mutant mice as they age although the mice still remain infertile. These data show that the possible impact of dietary phytoestrogens should be taken into account when studying the phenotype of mutant mice with defects in the reproductive axis.
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McFarlane, L., V. Truong, J. S. Palmer, and D. Wilhelm. "Novel PCR Assay for Determining the Genetic Sex of Mice." Sexual Development 7, no. 4 (2013): 207–11. http://dx.doi.org/10.1159/000348677.

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Suto, J. "Genetic analysis of inferior nurturing ability in RR mice." Reproduction 123, no. 1 (January 1, 2002): 52–58. http://dx.doi.org/10.1530/reprod/123.1.52.

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Astrof, Sophie, Andrew Kirby, Kerstin Lindblad-Toh, Mark Daly, and Richard O. Hynes. "Heart development in fibronectin-null mice is governed by a genetic modifier on chromosome four." Mechanisms of Development 124, no. 7-8 (August 2007): 551–58. http://dx.doi.org/10.1016/j.mod.2007.05.004.

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Vieira, A. R. "Oral Clefts and Syndromic Forms of Tooth Agenesis as Models for Genetics of Isolated Tooth Agenesis." Journal of Dental Research 82, no. 3 (March 2003): 162–65. http://dx.doi.org/10.1177/154405910308200303.

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Genetic defects responsible for tooth agenesis are only now beginning to be uncovered. MSX1 and PAX9 have been associated with tooth agenesis in mice and humans, but interestingly for humans, these genes are associated with specific missing teeth. Mouse models also show that specific genes contribute to the development of specific types of teeth. A precise description of the phenotype specifying which teeth are missing has become fundamental. Mendelian segregation can be identified in families with tooth agenesis, but heterogenous or multiple genes may be responsible for the development of specific types of teeth agenesis in humans. Data from animal models are still very complex, and the human embryology is still poorly understood. Oral clefts and syndromic forms of tooth agenesis may be the best models for isolated tooth agenesis. In the future, a precise description of the missing teeth in syndromes involving tooth agenesis may be useful.
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Tuffrey, M., F. Alexander, C. Woods, and D. Taylor-Robinson. "Genetic susceptibility to chlamydial salpingitis and subsequent infertility in mice." Reproduction 95, no. 1 (May 1, 1992): 31–38. http://dx.doi.org/10.1530/jrf.0.0950031.

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Dissertations / Theses on the topic "Mice embryology; mice genetics"

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McClellan, Kelly Anne. "Murine oocyte loss occurs during fetal development." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=79047.

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Recently, the timing of oocyte loss during murine development has been brought into question as authors using mouse vasa homologue (MVH) as a germ cell marker did not observe a loss of oocytes during fetal life. Instead the major loss was observed in the days following birth, after chromosome pairing has occurred.
In this study the controversy was addressed by establishing a new and reliable method to quantify murine oocytes in meiotic prophase, as well as to determine the gestation age and meiotic prophase stage of oocyte loss. Earlier limitations were overcome through the use of Germ Cell Nuclear Antigen-1 (GCNA-1) antibody as a germ cell specific marker, and the novel addition of a cytospin centrifugation step to the method. Progress through meiotic prophase was examined in chromosome spread preparations where meiotic stages were assessed using an antiserum against synaptonemal complex (SC) proteins. Quantification was accomplished by counting the number of GCNA-1 immunoreactive cells in chromosome spread preparations and estimated in histological sections using the ratio estimation model. (Abstract shortened by UMI.)
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Fu, Germaine 1976. "Mouse oocytes and embryos with or without the H10 gene : linker histone subtypes and development performance." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=33399.

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H1 histones are potentially significant to nuclear reprogramming during the oocyte-to-embryo transition. One characteristic distinguishing the H1 subtypes is that the somatic H1 histones are found primarily in dividing cells, whereas the H10 subtype is predominantly found in differentiated cells. The H1 complement in mouse oocytes and preimplantation embryos from wild-type and H10-/- animals was investigated.
Immunocytochemistry of wild-type cells demonstrated that H10 was predominant in oocytes while somatic H1 began accumulating in the 2-cell embryo. In H10-/- cells H10 was not detected, but, surprisingly, somatic H1 was detected beginning at the 1-cell stage. Radiolabeling of wild-type and H10-/- cells revealed that somatic H1 synthesis intensified after meiotic maturation, and therefore prior to its detection in embryos. The functional study found that loss of H10 impaired oogenesis but enhanced embryogenesis. The patterns of H1 immunodetection and synthesis are integrated, and the significance of H1 composition in development is discussed.
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McLay, David W. "Developmental regulation and molecular nature of an activity in murine oocytes that transfers histones onto sperm DNA." Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=38235.

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At fertilization, the remodelling of the sperm nucleus into the male pronucleus is critical for normal development. Morphological and functional changes to the nucleus are underpinned by biochemical changes in the chromatin composition, most notably the removal of sperm specific protamines and assembly of histones onto the paternal DNA. This exchange is controlled by oocyte factors, as exemplified in Xenopus by nucleoplasmin. Though mammalian factors remain unidentified, a functional assay based on antibodies recognizing core histones has been developed to test the activity in oocytes that transfers histones onto sperm DNA, named histone transfer activity (HTA). The assay was applied to growing and maturing murine oocytes to determine when during oogenesis HTA develops, and to probe potential regulatory mechanisms. Fully-grown oocytes develop HTA upon maturation, in a protein-synthesis dependent manner. Large, growing oocytes also develop HTA upon entry into M-phase. Small growing meiotically incompetent oocytes, ones that do not spontaneously enter M-phase, do not develop HTA, though this can be overcome by culture of oocytes to meiotic competence, or by treatment with strontium to induce intracellular calcium oscillations. Taken together these findings form a model of how HTA develops throughout oogenesis. Finally, an attempt is made to identify a potential mammalian HTA factor. Transcripts for two remodelling factors, mNAP and Npm3, are identified in the murine oocyte, and injection of anti-sense oligonucleotides reveals that Npm3 plays a significant role in the deposition of histories and the remodelling of sperm chromatin at fertilization. Combined with the findings of the HTA assay, the data forms a testable model of how Npm3 may be regulated throughout oogenesis.
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Macdonald, Karen Beth. "The genetics and embryopathology of exencephaly in SELH/Bc mice." Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/27983.

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This project was the first study of the genetics and embryo-pathology of exencephaly in a partially inbred mouse stock, SELH/Bc. Exencephaly was found in 17% of SELH fetuses. Analysis of day 8-9 gestation embryos indicated that SELH embryos were collectively normal in general development, but delayed in neural tube closure relative to overall or general development compared to two normal strains of mice, ICR/Be and SWV/Bc. Exencephaly was observed to be caused by a failure of fusion of the cranial neural folds in the mesencephalon region in SELH. All SELH embryos appeared to be abnormal in their pattern of cranial neural tube closure. They fail to make initial contact at the prosencephalon/mesencephalon junction region of the cranial neural folds (the first fusion in the cranial neural folds in normal embryos). SELH embryos, fused their anterior neural folds via an alternate (possibly passive) mechanism compared to normal strains of mice (SWV/Bc, and ICR/Be), by fusing the folds in a "zipper-like" fashion from the rostral base of the prosencephalon. This closure of the neural tube in genetically liable embryos by an abnormal sequence of events suggests a new model for anterior neural tube closure failure. Liability to exencephaly appeared to be fixed in the SELH stock. Of the 53 SELH males tested, all produced exencephaly. SELH animals were found to be heterogeneous in the frequency of exencephaly they produced, indicating that there are still genes segregating in the stock which affect the ability of embryos to complete anterior neural tube closure. Exencephaly in SELH does not appear to be caused by an autosomal dominant, sex-linked dominant or recessive, or simple autosomal recessive single gene, although F2, BCl, and BC2 exencephaly frequencies (after an outcross to ICR/Be) suggest that only a small number of genes are involved. A marked excess of female exencephalics was observed in SELH, F2, BCl, and BC2 fetuses.
Medicine, Faculty of
Medical Genetics, Department of
Graduate
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Moase, Connie E. (Connie Evelyn). "Histopathology of, and retinoic acid effects in, biochemically identified splotch-delayed mouse embryos." Thesis, McGill University, 1986. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=66099.

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Hurtubise, Patricia. "Intracellular signalling during murine oocyte growth." Thesis, McGill University, 2000. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=31239.

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During the growth phase of oogenesis, mammalian oocytes increase several hundred-fold in volume. Although it is known that ovarian granulosa cells send growth promoting signals, neither these external signals nor the transduction pathways that become activated in the oocyte are known. Therefore, the presence and the activity of candidate signaling pathways in growing murine oocytes were investigated. By immunoblotting, the MAP kinases, ERK1 and ERK2, as well as their activating kinase MEK, were detected in oocytes at all stages of growth. However, using a phospho-specific anti-ERK antibody, no immunoreactive species were detectable in isolated granulosa cells or oocytes at any stage of growth, except metaphase II. Phosphorylated ERK was also present, although in smaller quantities, in oocyte-granulosa cell complexes at the later stages of growth. Furthermore, when ovarian sections were stained with an anti-ERK antibody, the protein was found to be highly concentrated in the cytoplasm of oocytes at all stages of growth, with lower levels in the nucleus. Another member of the MAP kinase family, Jun kinase (JNK), was investigated. By immunoblotting, JNK was detected in growing oocytes. Experiments using an anti-JNK antibody on ovary sections revealed the protein to be uniformly distributed in non-growing and growing oocytes with no evidence of preferential nuclear localization. These results imply that an interaction between the oocyte and the granulosa cells may be required to generate phosphorylated ERK. They also imply that growth signals probably are not relayed through ERK, but do not exclude a role for Jun kinase in mediating oocyte growth.
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O'Leary, Debra Alison. "Characterisation of gene structure and function of the ETS transcription factor Gabpα in mouse." Monash University, Centre for Functional Genomics and Human Disease, 2003. http://arrow.monash.edu.au/hdl/1959.1/9445.

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Nowacka, Lidia. "Muscle gene transfer studies of a 27-BP segment of the troponin I fast gene IRE enhancer." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111563.

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The fast-skeletal-muscle-fiber-specific expression of the troponin I(fast) (TnIfast) gene is driven by an Intronic Regulatory Element (IRE) located within the first intron of the gene. The IRE is a 148 bp transcriptional enhancer that contains several known and suspected cis-regulatory elements. These include the E-box, the closely-spaced MEF2 site and CACT box, the CACC site, and the CAGG element. Previous loss-of-function studies performed using the quail TnIfast IRE suggest that its activity depended on the MEF2 and CACT elements. The goal of my thesis research was to determine whether the MEF2 and CACT sites were not only necessary, but also sufficient, to support IRE activity. I prepared head-to-tail multimers of a 27-bp IRE segment that consisted largely of the near-adjacent MEF2 and CACT elements and did not contain any other known/suspected elements. These multimers were cloned upstream of a reporter gene consisting of the minimal promoter of the quail TnIfast gene linked to sequences encoding human placental alkaline phosphatase. The transcriptional capabilities of the constructs were assessed by gene transfer into the mouse soleus muscle in vivo by intramuscular injection/electroporation, and histochemical analysis of reporter enzyme plap expression including quantitative microdensitometry. I found that expression of these constructs was readily detectable and that it was markedly reduced by prior mutation of the CACT and, especially, of the MEF2 sites. These data indicate that the short DNA segment containing MEF2 and CACT elements is sufficient to drive expression in skeletal muscle and confirms the functional importance of these specific elements.
Although constructs containing the wild-type IRE 27-bp region were expressed, there was little preferential expression in fast fibers, in contrast to expression driven by the complete 148-bp IRE. Thus my results indicate that the MEF2 and CACT elements are not sufficient to drive fast fiber-type-specific expression, and suggest that additional elements outside of the 27-bp region tested are also necessary for fiber-type-specificity.
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Glaser, Juliane. "Functional characterization of the imprinted Liz/Zdbf2 locus in mice : from the early embryo to adult physiology." Electronic Thesis or Diss., Sorbonne université, 2018. http://www.theses.fr/2018SORUS243.

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L’empreinte parentale est un mécanisme de régulation épigénétique qui réduit l’expression d’environ 120 gènes à une seule dose parentale. L’expression monoallélique dépend de marques différentielles de méthylation de l’ADN, établies dans l’ovocyte et le spermatozoïde et maintenues après fécondation dans l’individu en développement. Chez les mammifères, les gènes soumis à empreinte sont essentiels au développement embryonnaire et à certaines fonctions comportementales et physiologiques après la naissance. Définir les mécanismes de régulation et la fonction des gènes soumis à empreinte est une question cruciale en biologie du développement et en pathologie. Mon travail de thèse a concerné l’étude fonctionnelle du locus Zdbf2 chez la souris. Zdbf2 est un gène exprimé paternellement, conservé chez l’humain, mais dont la fonction était inconnue. J’ai pu démontrer que l’activation de Zdbf2 dans le cerveau de souris pré-pubères dépend d’un signal épigénétique indélébile mis en place dès les premiers jours de développement embryonnaire. Cette programmation précoce de Zdbf2 assure une croissance normale du nouveau-né. Mes résultats indiquent de plus que la dose, mais pas l’origine parentale de Zdbf2 est essentielle. Ces découvertes ont été possibles par la création de divers modèles mutants avec des variations de la dose de Zdbf2 dans l’axe hypothalamo-hypophysaire. Ce travail met en lumière la fonction cruciale d’un gène soumis à empreinte, de sa régulation dans l’embryon précoce à son rôle sur la physiologie adulte
Genomic imprinting refers to the epigenetic mechanism by which approximately 120 genes are expressed in a parent-of-origin manner. This parental asymmetry in gene expression is mediated through differential profiles of DNA methylation established in the oocyte and the sperm and maintained after fertilization in the developing individual. In mammals, imprinted genes are essential for normal embryo development as well as behavioral and physiological functions after birth. Clarifying the regulation and the function of those genes is thus fundamental in the field of developmental biology and health. During my PhD, I functionally characterized the imprinted Zdbf2 locus in mice. Zdbf2 is a paternally expressed gene, conserved from mouse to human, whose biological function was unknown. I revealed that Zdbf2 activation in the post-natal brain requires an indelible epigenetic signal that is established during the first days of embryogenesis. Additionally, I provided in vivo evidence that early programming of Zdbf2 is essential for proper growth after birth. By generating multiple CRISPR-mediated genetic mutants with varied doses of Zdbf2 in the hypothalamo-pituitary axis, I finally demonstrated that Zdbf2 is a growth-promoting gene, with a dose-sensitive effect and acting independently of its parental origin. Altogether, my work shed light onto the crucial function of a mammalian imprinted gene, from its regulation in the early embryo to its role in adult physiology
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Poirier, Luc. "The degradation of the stem-loop binding protein at the late 2-cell stage of mouse embryogenesis /." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=80351.

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The efficient processing of replication-dependent histone mRNA requires the Stem-Loop Binding Protein (SLBP). SLBP is also involved in regulating histone mRNA half-life, their nucleocytoplasmic transport, and their translation. Unlike somatic cells, where SLBP protein accumulates only in S-phase, SLBP protein is present throughout the first two embryonic cell cycles in mice. We report here that in late 2-cell mouse embryos there is a substantial, proteasome-dependent decrease in SLBP throughout the cell. Based on chromosome morphology, the degradation of SLBP protein in late 2-cell embryos is most likely a late G2-phase event. The degradation of SLBP protein is not simply a zygotic clock event, but requires development to the late 2-cell stage. Furthermore, SLBP protein degradation in 2-cell mouse embryos requires cyclin-dependent kinase (Cdk) activity, DNA replication, and zygotic genome activation. A model for SLBP protein degradation is proposed based on observations made in both early mouse embryos and somatic cells.
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Books on the topic "Mice embryology; mice genetics"

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service), ScienceDirect (Online, ed. Guide to techniques in mouse development: Mouse molecular genetics. Amsterdam: Elsevier /Academic Press, 2010.

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Hogan, Brigid. Manipulating the mouse embryo: A laboratory manual. Cold Spring Harbor, NY: Cold Spring Harbor Laboratory, 1986.

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1952-, Costantini Frank, and Lacy Elizabeth, eds. Manipulating the mouse embryo: A laboratory manual. Cold Spring Harbor, N.Y: Cold Spring Harbor Laboratory, 1986.

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Genetic analysis of animal development. New York: Wiley, 1986.

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Genetic analysis of animal development. 2nd ed. New York: Wiley-Liss, 1993.

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Gilmore, McKinnell Robert, ed. Cloning of frogs, mice, and other animals. Minneapolis: University of Minnesota Press, 1985.

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Silver, Lee M. Mouse genetics: Concepts and applications. New York: Oxford University Press, 1995.

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Bürki, Kurt. Experimental embryology of the mouse. Basel: Karger, 1986.

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L, Bard Jonathan B., ed. The anatomical basis of mouse development. San Diego, CA: Academic Press, 1999.

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The house mouse: Atlas of embryonic development. New York: Springer-Verlag, 1989.

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Book chapters on the topic "Mice embryology; mice genetics"

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Gaudilliere, Jean-Paul. "Circulating Mice and Viruses." In The Practices of Human Genetics, 89–124. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4718-7_4.

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Leder, P. "Transgenic Mice in the Study of Human Disease." In Human Genetics, 377. Berlin, Heidelberg: Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71635-5_47.

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Yunis, E. J., and M. Salazar. "Genetics of life span in mice." In Genetics and Evolution of Aging, 243–55. Dordrecht: Springer Netherlands, 1994. http://dx.doi.org/10.1007/978-94-017-1671-0_21.

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Maxson, Stephen C. "The Genetics of Offensive Aggression in Mice." In Handbook of Behavior Genetics, 301–16. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-76727-7_21.

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Kono, D. H., and A. N. Theofilopoulos. "Genetic Susceptibility to Spontaneous Lupus in Mice." In Genes and Genetics of Autoimmunity, 72–98. Basel: KARGER, 1999. http://dx.doi.org/10.1159/000060497.

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Ukai, Hideki, Koji L. Ode, and Hiroki R. Ueda. "Next-Generation Mice Genetics for Circadian Studies." In Circadian Clocks, 359–76. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-2577-4_17.

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Anderson, Lucy M., Marek A. Sipowicz, Wei Yu, Bhalchandra A. Diwan, Lisa Birely, Diana C. Haines, Charles W. Riggs, and Kazimierz S. Kasprzak. "Chromium(III) as a Male Preconception Carcinogen in Mice." In Metals and Genetics, 171–82. Boston, MA: Springer US, 1999. http://dx.doi.org/10.1007/978-1-4615-4723-5_12.

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Lovell-Badge, Robin, Clare Canning, and Ryohei Sekido. "Sex-Determining Genes in Mice: Building Pathways." In The Genetics and Biology of Sex Determination, 4–22. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/0470868732.ch2.

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D’Hoostelaere, L., K. Huppi, B. Mock, C. Mallett, D. Gibson, J. Hilgers, and M. Potter. "The Organization of the Immunoglobulin Kappa Locus in Mice." In Genetics of Immunological Diseases, 116–29. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-50059-6_18.

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Rubin, Edward, and Joshua Schultz. "Probing the Genetics of Atherosclerosis in Transgenic Mice." In Transgenic Animals as Model Systems for Human Diseases, 25–37. Berlin, Heidelberg: Springer Berlin Heidelberg, 1993. http://dx.doi.org/10.1007/978-3-662-02925-1_2.

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Conference papers on the topic "Mice embryology; mice genetics"

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Turner, Charles H., and Alexander G. Robling. "Genetic Effects on Skeletal Mechanosensitivity in Mice." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-32596.

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The accumulation of bone mass during growth can be enhanced by environmental factors such as mechanical loading (exercise) or calcium intake, but 60–70% of the variance in adult bone mineral density (BMD) is explained by heredity. Consequently, understanding the signaling pathways targeted by the genes governing bone accumulation holds perhaps the greatest potential in reducing fracture incidence later in life. Rodent models are particularly useful for studying the genetics of skeletal traits. Of the available inbred mouse strains, three in particular have been studied extensively in skeletal genetics: C57BL/6, DBA/2, and C3H/He. The C57BL/6 strain is characterized by low BMD and large total cross-sectional area (CSA) in the midshaft femur; the C3H/He strain exhibits very high femoral BMD and a smaller femoral CSA than the C57BL/6 mice; and DBA/2 mice have moderately high femoral BMD and a very small midshaft femur CSA. Mechanical loading of the skeleton during growth can substantially enhance periosteal bone apposition, and ultimately produce a diaphyseal cross section with enlarged area. Therefore we hypothesized that the mouse strain with greater femoral cross-sectional area (C57BL/6) might have a genetic predisposition for greater mechanosensitivity than mice with smaller cross sections (C3H/He and DBA/2).
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Ratnadiwakara, Madara, Rohan B. Williams, and Anneke C. Blackburn. "Abstract A117: Vitamin D, parathyroid hormone,Cyp2r1, and breast cancer susceptibility in mice." In Abstracts: AACR Special Conference on Advances in Breast Cancer Research: Genetics, Biology, and Clinical Applications - October 3-6, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1557-3125.advbc-a117.

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Turner, Charles H. "How Microimaging Technology Is Transforming the Field of Skeletal Genetics." In ASME 2002 International Mechanical Engineering Congress and Exposition. ASMEDC, 2002. http://dx.doi.org/10.1115/imece2002-33057.

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Microcomputed tomography (microCT) is emerging as the technique of choice for skeletal genetics research. The goal of these studies is to identify genes that modulate bone strength and skeletal biomechanics. Many studies use animal models, namely rats and mice. To fully characterize the skeletal phenotype, one must determine the size, shape, and microstructure of the bones preferably in three dimensions. In what follows are three examples of how μCT has been used to illuminate genetic effects on bone structure.
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"The effect of "early"protein of papillomavirus HPV16 E2 made in plant expression system on the base of tomato fruit on tumor formation in mice infected with cancer HeLa cells." In Plant Genetics, Genomics, Bioinformatics, and Biotechnology. Novosibirsk ICG SB RAS 2021, 2021. http://dx.doi.org/10.18699/plantgen2021-168.

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Kulik, M. J., D. S. Shenoda, and C. R. Forest. "A Low-Cost, Two-Axis, Precision Robot for Automated Fluorescence In-Situ Hybridization Assays." In ASME 2009 International Mechanical Engineering Congress and Exposition. ASMEDC, 2009. http://dx.doi.org/10.1115/imece2009-13272.

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Genetics research often relies on experiments that require repetitive, time-consuming handling of small volumes of liquid (1 mL) and biomass (10–20 μL) such as fluorescence in-situ hybridization (FISH), β-galactosidase staining, immunohisto chemistry, skeletal and tunel assays. Often manual, these experiments are time intensive and error-prone. We report on the design, fabrication, and testing of a low-cost, two-axis, precision robot for FISH assays on whole mice embryos. The robot can complete 20 successive embryo immersions in unique isothermal solutions in minutes for 6 samples. Repeatability of the orthogonal axes is 66 and 214 μm, near the measurement uncertainty limit and sufficient for operation. Accuracy is achieved by systematic error compensation. Low-cost and precision are obtained using design and manufacturing techniques and processes, resulting in a cost of 15% of comparable instruments (e.g., InsituStain, Intavis Bioanalytical Instruments). This design demonstrates a simple, automated platform to perform a typically manual experimental genetics technique.
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Reports on the topic "Mice embryology; mice genetics"

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Blank, Robert D. Genetics of Bone Mineralization and Morphology in Inbred Mice: Analysis of the HcB/Dem Recombinant Congenic Strains. Fort Belvoir, VA: Defense Technical Information Center, April 2001. http://dx.doi.org/10.21236/ada400522.

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