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Dissertations / Theses on the topic 'Mice Notch genes Mice'

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Published: 4 June 2021

Last updated: 12 February 2022

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1

Ruivenkamp, Claudia Antoinette Laetitia. "Colon cancer susceptibility genes in mice and humans." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2003. http://dare.uva.nl/document/67685.

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2

Jakt, Lars Martin. "Isolation of mouse Hoxb-3 protein binding sequences : a whole genome approach /." Thesis, Hong Kong : University of Hong Kong, 1999. http://sunzi.lib.hku.hk/hkuto/record.jsp?B21185505.

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3

Rigby, Robert James. "The identification of lupus susceptibility genes in New Zealand mice." Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.429877.

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4

Randhawa, J. S. "Molecular characterisation of the pneumonia virus of mice glycoprotein genes." Thesis, University of Warwick, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.387336.

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5

Boukouvala, Sotiria. "Expression of the genes for arylamine N-acetyltransferases in mice." Thesis, University of Oxford, 2002. http://ora.ox.ac.uk/objects/uuid:ed864a10-2cb9-4ebe-8a2c-934d707c5a0d.

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6

Freland, Sofia. "Lymphoid development and function in MHC class I deficient mice /." Stockholm, 1999. http://diss.kib.ki.se/1999/91-628-3714-1/.

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7

Keshavarz, Maryam [Verfasser]. "Analysis of candidate genes for behavioral differences in mice / Maryam Keshavarz." Kiel : Universitätsbibliothek Kiel, 2019. http://d-nb.info/1187242616/34.

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8

Faulkes, David Julian. "The analysis of human serum amyloid A genes using transgenic mice." Thesis, Open University, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.287010.

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9

Scherer, Christina Ann. "An in vitro screen to isolate developmentally regulated genes in mice." Thesis, Massachusetts Institute of Technology, 1995. http://hdl.handle.net/1721.1/32638.

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10

Dershem, Victoria Lynne. "The Expression of Dopamine-Related Genes and Behavioral Performance in Mice." Wright State University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=wright1484217370390211.

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11

Narita, Makiko. "Genetic analysis of Nakano cataract and its modifier genes in mice." Kyoto University, 2002. http://hdl.handle.net/2433/149358.

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12

Bennetts, Jennifer. "The identification and characterisation of novel genes in development /." [St. Lucia, Qld.], 2006. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe19375.pdf.

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13

凌錦榮 and Kam-wing Ling. "Study of transgenic mice ectopically expressing the mouse Hoxb-3 gene." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31238993.

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14

Ling, Kam-wing. "Study of transgenic mice ectopically expressing the mouse Hoxb-3 gene /." Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B20735212.

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15

Berger, Caroline [Verfasser], and Ilse [Akademischer Betreuer] Hofmann. "Blockade of endothelial Notch signaling in cellular systems and adult mice / Caroline Berger ; Betreuer: Ilse Hofmann." Heidelberg : Universitätsbibliothek Heidelberg, 2013. http://d-nb.info/1177810220/34.

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16

Lemay, Anne-Marie. "Identification of bleomycin and radiation-induced pulmonary fibrosis susceptibility genes in mice." Thesis, McGill University, 2010. http://digitool.Library.McGill.CA:8881/R/?func=dbin-jump-full&object_id=92173.

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17

Farahani, Poupak. "Identification of novel candidate obesity genes in hepatic lipase knockout BSB mice /." For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2003. http://uclibs.org/PID/11984.

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18

Wentworth, Bruce Martin. "Characterization of the Two Non-Allelic Preproinsulin Genes in Mice: a Thesis." eScholarship@UMMS, 1987. http://escholarship.umassmed.edu/gsbs_diss/290.

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The two non-allelic preproinsulin genes of the mouse have been cloned and their nucleotide sequences determined. The mouse preproinsulin I gene, like its rat counterpart, has only one intron. Homology between the two mouse genes extends in the 5' direction to about position -500. Homology 3' of the coding sequence terminates shortly after the polyadenylation signal with a dA rich region found in gene I. The coding sequences of the two genes have been compared. The deduced amino acid sequences of the mature hormones are identical to the published protein sequences and to the corresponding sequences of rat insulins I and II. The prepeptides of mouse insulin I and II differ at six positions. However, they maintain hydrophobic cores that are required for transport of the nacent peptide across microsomal membranes. The B-peptide of mouse insulin I differs from insulin II at two positions: at position B9 a proline has replaced a serine, and at position B29 a lysine has replaced a methionine, compared to the sequence of insulin II. The A-peptides of the two hormones are identical. The C-peptide of mouse proinsulin I has a deletion eliminating amino acids C17 (Gly) and C18 (Ala) compared to the sequence of proinsulin II. The presence of this deletion in mature RNA was confirmed through an S1 nuclease assay. The transcriptional start sites for the preproinsulin genes were determined with S1 and Mung Bean nuclease assays, and with a primer extension assay. The data indicate that transcription of the mouse preproinsulin genes starts 6 bp 5' of the site reported for the rat II gene. Single-stranded DNA probes were used to determine the structure of the 3' ends of the preproinsulin mRNAs. Hybridization conditions were used which only allowed each probe to detect its cognate mRNA. Digestion of the resulting DNA-RNA duplex molecules with S1 nuclease followed by gel electrophoresis demonstrated that transcription of mouse preproinsulin I mRNA terminates 18 bases after the polyadenylation signal. Transcription of preproinsulin II mRNA terminates 43 bases after the polyadenylation signal, thus extending 25 bases past the last point of homology between the two genes. The 3' end-specific probes were used in experiments designed to determine the ratio of preproinsulin I and II mRNA in pancreatic extracts of normal, fasted and fasted and refed mice. In all cases the amount of preproinsulin I mRNA exceeded preproinsulin II by about 2.3:1. These results were extended to include an analysis of preproinsulin mRNA from freshly isolated islets and islets incubated for 48 hours in the presence of 2.8 mM or 16.7 mM glucose. With both high and low glucose concentrations, the amount of preproinsulin I mRNA exceeded preproinsulin II by about 2.3:1. The mouse islets were also incubated with 3H-leucine and the ratio of insulin I and II determined after fractionation by HPLC. Unlike the mRNA results, the level of insulin II, within the islets and secreted into the media, exceeded insulin I by about 2:1 under all conditions. The available preproinsulin prepeptide amino acid sequences have been compared. The sequence of mouse I prepeptide differs from most other insulin prepeptides at amino acid position 4. At that position a tryptophan residue that is conserved in most insulin prepeptides has been replaced by a leucine in the mouse I prepeptide. This change causes a shift in the hydropathy profile in that region of the mouse insulin I prepeptide making it more hydrophobic. Every other insulin prepeptide is relatively hydrophilic at that position. This difference is postulated to interfere with signal recognition particle mediated regulation of translation and/or transport of nacent mouse preproinsulin I to microsomal membranes, and nay account for the discordant mRNA-peptide ratios. The structure of the insulin genes in a number of myomorph rodents has been examined. The data indicate that only members of the sub-family Murinae have two insulin genes.

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19

Gilbert, Erin V. "Characterization of the Circadian Clock in Pet-1 Knockout Mice." Kent State University / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=kent1290535254.

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20

Brown, Raquel Monique. "RHOX GENES FUNCTION DURING FOLLICULOGENESIS." OpenSIUC, 2011. https://opensiuc.lib.siu.edu/theses/725.

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Mammalian ovulation is a complex, hormone-dependent developmental program in which several events must take place in an ordered progression to ensure that the oocyte is competent for fertilization. This process requires the coordinated expression of many genes which must be turned on and off in the right place at the right time for proper development of the follicle. While the hormone signals from the brain that initiate ovulation are known, the master control genes which regulate this process are not well known. Homeobox proteins are potential candidates to perform as master regulators. Homeobox proteins are DNA-binding proteins that regulate the transcription of downstream genes and thereby control biological events. We recently identified a new homeobox gene cluster on the mouse X chromosome that are only expressed in reproductive tissues. These reproductive homeobox (Rhox) homeobox genes are expressed in the ovary, placenta, testis, and epididymis, and thus are good candidates to regulate both male and female reproductive tissue development and physiology. Rhox gene expression fell into three categories: Class I exhibited peak expression prior to ovulation (0-8 hours after hCG), Class II were predominantly expressed during ovulation (8-16 hours after hCG), and Class III peaked after ovulation. The slightly overlapping windows of peak Rhox gene expression suggest that these genes may regulate specific events during the ovulatory cycle. The founding member of the cluster, Rhox5, is highly expressed in granulosa cells of pre-ovulatory follicles. We previously reported that Rhox5-null female mice are viable and fertile, suggesting that RHOX5 is either not essential for ovulation, or that one of the other RHOX factors may compensate functionally in granulosa cells. In order to identify potentially redundant RHOX factors, we examined the expression patterns of all 32 Rhox genes using an eCG primed, hCG induced superovulation model, in wild-type, Rhox5-null, and heterozygous littermate mice. Expression levels of Rhox1, exhibited peak expression prior to being hormonal primed, was reduced in the Rhox5-null animal. However, Rhox8 mRNA and protein were reduced at 2h and 4h post hCG, but recovered once the follicles passed the antral stage of development. Conversely, in progesterone receptor knockout mice (PRKO), Rhox8 exhibited normal stimulation by eCG, but failed to reach its peak mRNA level at 8h post-hCG found in WT mice. This suggests a model in which Rhox8 transcription is dependent upon RHOX5 during early folliculogenesis and progesterone during the periovulatory window when RHOX5 normally wanes. Subsequent promoter analysis in granulosa cells revealed essential homeobox binding and progesterone response elements within Rhox8's 5'-flanking region. Transfection of RHOX5 and PGR expression plasmids stimulated, whereas dominant negative and mutant constructs inhibited, Rhox8 promoter activity. At present, the specific impact of misregulation of Rhox5 and Rhox8 during early folliculogenesis is not known. However, follicle counts from serially sectioned ovaries, extirpated from normal cycling animals, indicated that Rhox5-null mice possess ~50% fewer follicles than heterozygous littermates. Loss of RHOX5 in Sertoli cells results in male subfertility characterized by poor germ cell survival due in part to the misregulation of metabolism promoting genes. One of these genes, Ins2, is also stimulated by RHOX5 and RHOX8 in granulosa cells, suggesting impaired insulin signaling may contribute reduced follicle development in Rhox5-null ovaries.

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21

Cheng, Qiao. "Genes regulating small-for-size fatty liver graft injury." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43085775.

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22

Mak, Siu-shan Suzanne. "Analysis of transgenic mice with ectopic Hoxb-3 expression in rhombomere 4 /." Hong Kong : University of Hong Kong, 2000. http://sunzi.lib.hku.hk/hkuto/record.jsp?B22079178.

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23

Vollersen, Nele Mareike [Verfasser], and Thorsten [Akademischer Betreuer] Schinke. "Characterization of genetically modified mice carrying pathogenic mutations in the Notch2 or Wnt1 gene / Nele Mareike Vollersen ; Betreuer: Thorsten Schinke." Hamburg : Staats- und Universitätsbibliothek Hamburg, 2019. http://d-nb.info/1179362632/34.

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24

Plucińska, Kaja. "Modelling Alzheimer's disease : the impact of genes and dietary manipulations in transgenic mice." Thesis, University of Aberdeen, 2014. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=218288.

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25

Joshi, Shreyas. "IDENTIFICATION OF NOVEL SLEEP RELATED GENES FROM LARGE SCALE PHENOTYPING EXPERIMENTS IN MICE." UKnowledge, 2017. http://uknowledge.uky.edu/biology_etds/42.

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Humans spend a third of their lives sleeping but very little is known about the physiological and genetic mechanisms controlling sleep. Increased data from sleep phenotyping studies in mouse and other species, genetic crosses, and gene expression databases can all help improve our understanding of the process. Here, we present analysis of our own sleep data from the large-scale phenotyping program at The Jackson Laboratory (JAX), to identify the best gene candidates and phenotype predictors for influencing sleep traits. The original knockout mouse project (KOMP) was a worldwide collaborative effort to produce embryonic stem (ES) cell lines with one of mouse’s 21,000 protein coding genes knocked out. The objective of KOMP2 is to phenotype as many as of these lines as feasible, with each mouse studied over a ten-week period (www.mousephenotype.org). The phenotyping for sleep behavior is done using our non-invasive Piezo system for mouse activity monitoring. Thus far, sleep behavior has been recorded in more than 6000 mice representing 343 knockout lines and nearly 2000 control mice. Control and KO mice have been compared using multivariate statistical approaches to identify genes that exhibit significant effects on sleep variables from Piezo data. Using these statistical approaches, significant genes affecting sleep have been identified. Genes affecting sleep in a specific sex and that specifically affect sleep during daytime and/or night have also been identified and reported. The KOMP2 consists of a broad-based phenotyping pipeline that consists of collection of physiological and biochemical parameters through a variety of assays. Mice enter the pipeline at 4 weeks of age and leave at 18 weeks. Currently, the IMPC (International Mouse Phenotyping Consortium) database consists of more than 33 million observations. Our final dataset prepared by extracting biological sample data for whom sleep recordings are available consists of nearly 1.5 million observations from multitude of phenotyping assays. Through big data analytics and sophisticated machine learning approaches, we have been able to identify predictor phenotypes that affect sleep in mice. The phenotypes thus identified can play a key role in developing our understanding of mechanism of sleep regulation.

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26

麥小珊 and Siu-shan Suzanne Mak. "Analysis of transgenic mice with ectopic Hoxb-3 expression in rhombomere 4." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2000. http://hub.hku.hk/bib/B31223175.

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27

Cheung, Kwan-lok. "Analysis of lacZ gene expression patterns of a Hoxb3[lacZ] mouse mutant during early development /." View the Table of Contents & Abstract, 2005. http://sunzi.lib.hku.hk/hkuto/record/B3508571X.

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28

Wong, Raymond, and 黃偉文. "Generation and characterization of polyclonal antibodies specific to the mouse homeodomain protein HOXB-3." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B31221968.

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29

Ng, Shuk-ming Sandy. "A study on the production of transgenic mice by pronuclear microinjection and by sperm incorporation of immunoglobulin genes /." [Hong Kong : University of Hong Kong], 1992. http://sunzi.lib.hku.hk/hkuto/record.jsp?B13215905.

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30

Kwan, Chung-tin. "Studies of the regulation of mouse Hoxb-3 gene /." Hong Kong : University of Hong Kong, 1998. http://sunzi.lib.hku.hk/hkuto/record.jsp?B20666871.

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31

Cheng, Qiao, and 程喬. "Genes regulating small-for-size fatty liver graft injury." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43085775.

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32

Hosokawa, Shinichi. "Impact of Sox9 Dosage and Hes1-mediated Notch Signaling in Controlling the Plasticity of Adult Pancreatic Duct Cells in Mice." Kyoto University, 2015. http://hdl.handle.net/2433/200490.

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33

Masadah, Rina. "Generation of transgenic mice overexpressing human Smoothened and human GLI1 genes in their skin /." [St. Lucia, Qld.], 2006. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe19678.pdf.

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34

Howard, Lorraine Tamar. "The construction and characterization of hypoxia responsive reporter genes for use in transgenic mice." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/MQ63131.pdf.

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35

De, Kumar Bony. "Induction of Hox genes and genome wide identification of Hox binding sites in mice." Thesis, Open University, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607467.

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Hox genes encode a family of transcription factors that play highly conserved regulatory roles in specifying the properties of tissues in developing embryos. Very little is known about how HOX proteins control the cellular and developmental processes governing morphogenesis through regulation of down-stream target genes. The goal of this research was to investigate on a genome-wide basis, the rules and principles which underlie the binding of different HOX proteins to target sites and understand the basis for their distinct specificities. I utilized the programmed differentiation of mouse embryonic stem cells into a neural fate with retinoids and genomic technologies to systematically investigate binding properties of two HOX proteins, HOXA1 and HOXBI and their cofactors PBX and MEIS. I analyzed the induction properties of the cells and the transcriptional dynamics and epigenetic states in Hox clusters to explore the differentiation process. An extensive and dynamic pattern of transcriptional activity indicates that Hox clusters generate a large number of non-coding RNAs which may impact their activation and chromatin states. Global identification of HOXB 1, HOXA1, PBX and MEIS binding regions by chromatin immune precipitation and high throughout sequencing (ChIP-seq) has generated insight into many potential Hox target genes. HOXA1 binding peaks generally overlapped with those of PBX and MEIS, supporting their roles as HOX co-factors. The sites bound by HOXBl uncovered new classes of binding motifs. Regulatory assays demonstrated that many of these novel motifs functioned as neuronal enhancers. Many HOXB I binding peaks have closely associated REST motifs and bind the REST repressor complex, which is important in neuronal differentiation. The close association of REST and HOXB 1 binding sites provides a mechanism for coordinating cell differentiation programs in neurogenesis. This research has uncovered novel properties of HO X proteins and their co-factors that underlie their role as master regulators of patterning and morphogenesis

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36

Kam, Ka-man, and 甘嘉敏. "Expression of engrailed-Hoxb5 transcriptional repressor by Wnt1-Cre produces neurocristopathies in mice." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47155735.

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Neural crest cells (NCC) arise from the neural tube (NT) and migrate through given regions of embryos, where they generate most of the peripheral nervous system (PNS), facial skeleton and pigment cells. Defective NCC development gives rises to malformations in multiple NCC-derived structures, collectively known as neurocristopathies. NCC from the NT vagal and trunk levels express Hoxb5 plus a number of other Hox proteins. Hoxb5 is a member of Hox transcription factors family that binds to specific target nucleotide sequences in the genome via their DNA-binding domain, where they regulate gene expressions. Vagal NCC migrate to the intestine and generate the enteric nervous system (ENS). To test the Hoxb5 function in vagal NCC, we made use a transgenic mouse line (enb5) and showed that perturbation of Hoxb5 signaling in NCC resulted in down-regulation of Ret and defective ENS, indicating that normal Hoxb5 function was required for the development of vagal NCC. Current project aims to investigate the function of Hoxb5 in trunk NCC development. Transgenic mouse enb5 can be induced by Cre recombinase to express a hybrid protein namely engrailed-Hoxb5 (enb5), in which the transactivation domain of the mouse Hoxb5 is replaced with a repressor domain of the Drosophila engrailed (en) protein. With the intact DNA-binding domain, enb5 binds to target genes of Hoxb5, repressing the expression of target genes instead of induction. Therefore, enb5 produces a dominant negative effect on the developmental pathways that normally require Hoxb5. In this study, enb5 mice were crossed to Wnt1-Cre mice to express enb5 in NCC that arose from the entire length of NT. Wnt1-Cre/enb5 mutants displayed apoptosis of NCC, skin hypopigmentation and PNS defects (hypoplastic dorsal root ganglion and defective ENS). Expression of Sox9, Foxd3 and Ret was down-regulated in Wnt1-Cre/enb5 embryos. Conditional deletion of Sox9 and Foxd3 by Wnt1-Cre, or conventional deletion of Ret in mice produced NCC phenoptypes similar to those of Wnt1-Cre/enb5. Taken all these prompted me to further investigate if Hoxb5 functioned in the same pathway as Sox9 and Foxd3 for NCC development using multiple experimental approaches. In ovo electroporation of enb5 in chick embryos induced apoptosis of NT, and co-electroporation of Hoxb5, Ret, Sox9 or Foxd3 rescued enb5-induced cell death. By bioinformatics analysis, Hoxb5 binding sites were identified in SOX9 and FOXD3 promoter sequences. Binding of Hoxb5 protein onto these binding sites of SOX9 and FOXD3 promoters was revealed by electro-mobility shift assay and further confirmed by chromatin immuno-precipitation assay. In addition, enb5 was also shown to bind to the same regions of SOX9 and FOXD3 promoters as Hoxb5. Using dual luciferase reporter assay, Hoxb5 was shown to induce transcription from SOX9 and FOXD3 promoters, and enb5 blocked the induction. Taken all these indicate that (i) Hoxb5 binds and induces transcriptions from SOX9 and FOXD3 promoters, (ii) enb5 blocks the induction. In summary, Hoxb5 regulates NCC development by controlling the expression of Sox9, Foxd3 and Ret, and perturbation of Hoxb5 signaling results in NCC death and neurocristopathies.
published_or_final_version
Surgery
Doctoral
Doctor of Philosophy

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37

Sae-Pang, Jearn Jang, and 彭淦長. "Craniofacial abnormalities in transgenic mice with ectopic expression of the Hoxb-3 gene." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2002. http://hub.hku.hk/bib/B31227818.

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38

鄧焯安 and Cheuk-on Tang. "A study of clonality of lymphoma of SJL mice using immunoglobulin generearrangements and murine leukaemia virus integration." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1996. http://hub.hku.hk/bib/B31213650.

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39

Liu, Yuchen, and 刘雨辰. "The roles of Irx3 and Irx5 genes in mammalian inner ear development." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hdl.handle.net/10722/207900.

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Iroquois genes encode a family of highly conserved TALE homeodomain transcription factors that are involved in multiple developmental processes. Physiological tests indicated that Irx3 and Irx5 mutant mice displayed hearing impairment. However, the functions of these two genes during inner ear development are not known. The aim of this study is to characterize the roles of Irx3 and Irx5 during mammalian inner ear development using mouse models, in order to reveal the underlying mechanism for the hearing abnormality in the mutants. Two mouse mutants, Irx3tauLacZ and Irx3flox5EGFP with β-gal and EGFP reporters, were analyzed to examine the expression of these two genes in the otic vesicle and cochlear epithelium. In the otocyst, both Irx3 and Irx5 were expressed in the ventral-medial region. Irx5 expression was restricted to the non-sensory domain of the cochlear epithelia, while Irx3 was widely expressed, including the auditory sensory organ, the organ of Corti. The overlapping expression patterns of Irx3 and Irx5 suggest that they may share redundant functions. To investigate the roles of Irx3 and Irx5 during inner ear development, phenotypic analysis was performed on Irx3-/-, Irx5-/- and Irx3/5-/- mutant embryos. As shown by paint-filling analysis, Irx3/5-/- displayed shortened cochlear duct, enlarged cochlear lumen with fused sensory organ. Whole-mount phalloidin staining of hair cell bundles showed that Irx3-/- displayed occasional ectopic inner hair cells. Moreover, only supernumerary vestibular hair cell-like cells were developed in Irx3/5-/- mutant. These results suggest that Irx3 and Irx5 are required for inner ear morphogenesis and the formation of organ of Corti. To understand the effect of Irx3 and Irx5 in the cellular patterning of the cochlea, mutant cochleae were analyzed with markers for different regions of the cochlear epithelia. Altered expression domain of MyoVIIa, Sox2 and Gata2 in Irx3/5-/- cochlea revealed that the boundary between the Kolliker’s organ and the organ of Corti was lost and the location of sensory and non-sensory region was shifted. These results imply that Irx3 and Irx5 function in the establishment of the sensory/non-sensory boundary. It is known that p27kip1 regulates the wave of cell cycle exit in the developing organ of Corti and Sox2 takes part in prosensory specification. To explore the underlying reason for the patterning defects in Irx3/5-/- mutant, cochlear duct from prosensory stages were analyzed. Irx3/5-/- showed altered Sox2 and p27kip1 expression, with expanded prosensory domain and disrupted cell cycle exit. Ectopic prosensory proliferation was detected in the middle turn of the cochlear duct at E13.5 by BrdU incorporation assay. Therefore, Irx3 and Irx5 may participate in the subdivision of sensory territory in developing cochlea by controlling prosensory proliferation. In summary, this study demonstrates that Irx3 and Irx5 cooperate in multiple aspects of inner ear development: an early role to regulate prosensory proliferation and cell cycle exit; a second role to regulate cellular patterning of the cochlear duct by controlling the setting of sensory/non-sensory boundaries in the cochlea; a later role to regulate inner ear morphogenesis. This study supports the idea that Irx3 and Irx5 act as patterning genes during vertebrate evolution.
published_or_final_version
Biochemistry
Master
Master of Philosophy

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40

Hung, Siu-chun. "Analysis of abnormal branchial arch structures of a Hoxb3 transgenic mouse mutant using a lacZ Reporter mouse line." Click to view the E-thesis via HKUTO, 2004. http://sunzi.lib.hku.hk/hkuto/record/B31971830.

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41

Sae-Pang, Jearn Jang. "Analysis of multiple cardiac abnormalities in a Boxb3 mouse mutant." View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B37231194.

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42

Hung, Siu-chun, and 洪少俊. "Analysis of abnormal branchial arch structures of a Hoxb3 transgenic mouse mutant using a lacZ Reporter mouse line." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B31971830.

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43

吳淑明 and Shuk-ming Sandy Ng. "A study on the production of transgenic mice by pronuclear microinjection and by sperm incorporation of immunoglobulin genes." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1992. http://hub.hku.hk/bib/B31210521.

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44

關仲天 and Chung-tin Kwan. "Studies of the regulation of mouse Hoxb-3 gene." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31237150.

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45

Cheung, Kwan-lok, and 張君樂. "Analysis of lacZ gene expression patterns of a Hoxb3[lacZ] mouse mutant during early development." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2005. http://hub.hku.hk/bib/B45010596.

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46

Tang, Cheuk-on. "A study of clonality of lymphoma of SJL mice using immunoglobulin gene rearrangements and murine leukaemia virus integration /." Hong Kong : University of Hong Kong, 1996. http://sunzi.lib.hku.hk/hkuto/record.jsp?B16064823.

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47

Margaryan, Edith. "Expression of SIX3, ZFP161 and ALK Genes in the Brain and Kidneys of3H1 Br Mutant Mice." Thesis, University of Hawaii at Manoa, 2002. http://hdl.handle.net/10125/6950.

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Abstract:

A newly identified mouse mutation, called Br, displays heritable phenotypic features of frontonasal dysplasia (FND) and multic0ystic renal hypodysplasia (MRHD). The Br mutation is mapped to distal murine chromosome 17, but the causative gene remains unknown. The objective of this project was to analyze expression of three positional candidate genes, Six3, Zfp161 and ALK, in their target tissues. Two of these genes, Six3 and the putative mouse TGIF homologue, Zfp161, are candidates for the neurodevelopmental disorder, holoprosencephaly (HPE). Previous reports indicate a possible pathogenic relationship between HPE and FND, implicating HPE candidate genes in development of FND. The third gene of interest, ALK, is a neural developmental gene, also involved in renal morphogenesis. Embryos were collected on gestational day (GD) 18, and brain and kidney tissues were extracted. RT-PCR experiments were performed and expression was visualized with ethidium bromide staining. All three genes were found to be expressed in all examined tissues. Expression of the Six3 gene in the kidney was not previously described in the literature. This implies a novel role of Six3 in the renal development. Detailed mutational analysis of identified Six3 expression will be useful for evaluating its role in Br mutation.
xiii, 56 leaves

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Wong, Kung-yen Corinne, and 黃共欣. "Analysis of abnormal phenotypes of Hoxb3 mouse mutants generated by gene targeting." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B29158904.

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Wallén, Helena. "Olfactory sensitivity in CD-1 mice for six L- and D amino acids." Thesis, Linköping University, Department of Physics, Chemistry and Biology, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-56783.

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Sullivan, Kyle Alexander. "Paclitaxel Chemotherapy and Mammary Tumors Independently Disrupt Circadian Rhythmicity in Mice." The Ohio State University, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu1593640160389267.

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