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MausDB: An open source application for phenotype data and mouse colony management in large-scale mouse phenotyping projects
<span title="">2008</span>
<i title="Springer Nature">
<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/n5zrklrhlzhtdorf4rk4rmeo3i" style="color: black;">BMC Bioinformatics</a>
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Large-scale, comprehensive and standardized high-throughput mouse phenotyping has been established as a tool of functional genome research by the German Mouse Clinic and others. In all these projects, vast amounts of data are continuously generated and need to be stored, prepared for data-mining procedures and eventually be made publicly available. Thus, central storage and integrated management of mouse phenotype data, genotype data, metadata and linked external data are highly important.
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<a target="_blank" rel="external noopener noreferrer" href="https://doi.org/10.1186/1471-2105-9-169">doi:10.1186/1471-2105-9-169</a>
<a target="_blank" rel="external noopener" href="https://www.ncbi.nlm.nih.gov/pubmed/18366799">pmid:18366799</a>
<a target="_blank" rel="external noopener" href="https://pubmed.ncbi.nlm.nih.gov/PMC2292142/">pmcid:PMC2292142</a>
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... rements most probably depend on the individual mouse housing unit or project and the demand for either very specific individual database solutions or very flexible solutions that can be easily adapted to local demands. Not every group has the resources and/or the know-how to develop software for this purpose. A database application has been developed for the German Mouse Clinic in order to meet all requirements mentioned above. Results: We present MausDB, the German Mouse Clinic web-based database application that integrates standard mouse colony management, phenotyping workflow scheduling features and mouse phenotyping result data management. It links mouse phenotype data with genotype data, metadata and external data such as public web databases, which is a prerequisite for comprehensive data analysis and mining. We describe how this can be achieved with a lean and user-friendly system built on open standards. Conclusion: MausDB is suited for large-scale, high-throughput phenotyping facilities but can also be used exclusively for mouse colony management within smaller units or projects. The system is successfully used as the primary mouse and data management tool of the German Mouse Clinic and other mouse facilities. We offer MausDB to the scientific community as open source software to provide a system for storage of data from functional genomics projects in a well-structured, easily accessible form.
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Cold spells in the Nordic Seas during the early Eocene Greenhouse
<span title="2020-09-18">2020</span>
<i title="Springer Science and Business Media LLC">
<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/a4wan6l5o5dfzn767kyz7jqevi" style="color: black;">Nature Communications</a>
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The early Eocene (c. 56 - 48 million years ago) experienced some of the highest global temperatures in Earth's history since the Mesozoic, with no polar ice. Reports of contradictory ice-rafted erratics and cold water glendonites in the higher latitudes have been largely dismissed due to ambiguity of the significance of these purported cold-climate indicators. Here we apply clumped isotope paleothermometry to a traditionally qualitative abiotic proxy, glendonite calcite, to generate
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... temperature estimates for northern mid-latitude bottom waters. Our data show that the glendonites of the Danish Basin formed in waters below 5 °C, at water depths of <300 m. Such near-freezing temperatures have not previously been reconstructed from proxy data for anywhere on the early Eocene Earth, and these data therefore suggest that regionalised cool episodes punctuated the background warmth of the early Eocene, likely linked to eruptive phases of the North Atlantic Igneous Province.
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EuroPhenome: a repository for high-throughput mouse phenotyping data
<span title="2009-11-23">2009</span>
<i title="Oxford University Press (OUP)">
<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/hfp6p6inqbdexbsu4r7usndpte" style="color: black;">Nucleic Acids Research</a>
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Clinical Chemistry Reference Intervals for C57BL/6J, C57BL/6N, and C3HeB/FeJ Mice (Mus musculus)
<span title="">2016</span>
<i title="American Association for Laboratory Animal Science">
<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/726ldb3zong3vjkvay7tmblnme" style="color: black;">Journal of the American Association for Laboratory Animal Science</a>
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Although various mouse inbred strains are widely used to investigate disease mechanisms and to establish new therapeutic strategies, sex-specific reference intervals for laboratory diagnostic analytes that are generated from large numbers of animals have been unavailable. In this retrospective study, we screened data from more than 12,000 mice phenotyped in the German Mouse Clinic from January 2006 through June 2014 and selected animals with the genetic background of C57BL/6J, C57BL/6N, or
<span class="external-identifiers">
<a target="_blank" rel="external noopener" href="https://www.ncbi.nlm.nih.gov/pubmed/27423143">pmid:27423143</a>
<a target="_blank" rel="external noopener" href="https://pubmed.ncbi.nlm.nih.gov/PMC4943607/">pmcid:PMC4943607</a>
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... /FeJ. In addition, we distinguished between the C57BL/6NTac substrain and C57BL/6N mice received from other vendors. The corresponding data sets of electrolytes (sodium, potassium, calcium, chloride, inorganic phosphate), lipids (cholesterol, triglyceride), and enzyme activities (ALT, AST, ALP, α-amylase) and urea, albumin, and total protein levels were analyzed. Significant effects of age and sex on these analytes were identified, and strain- or substrain- and sex-specific reference intervals for 90- to 135-d-old mice were calculated. In addition, we include an overview of the literature that reports clinical chemistry values for wild-type mice of different strains. Our results support researchers interpreting clinical chemistry values from various mouse mutants and corresponding wild-type controls based on the examined strains and substrains.
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Principles and application of LIMS in mouse clinics
<span title="2015-07-25">2015</span>
<i title="Springer Nature">
<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/2wcheulsyvd7bott7zn35dhoti" style="color: black;">Mammalian Genome</a>
</i>
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Large-scale systemic mouse phenotyping, as performed by mouse clinics for more than a decade, requires thousands of mice from a multitude of different mutant lines to be bred, individually tracked and subjected to phenotyping procedures according to a standardised schedule. All these efforts are typically organised in overlapping projects, running in parallel. In terms of logistics, data capture, data analysis, result visualisation and reporting, new challenges have emerged from such projects. These challenges could hardly be
<span class="external-identifiers">
<a target="_blank" rel="external noopener noreferrer" href="https://doi.org/10.1007/s00335-015-9586-7">doi:10.1007/s00335-015-9586-7</a>
<a target="_blank" rel="external noopener" href="https://www.ncbi.nlm.nih.gov/pubmed/26208973">pmid:26208973</a>
<a target="_blank" rel="external noopener" href="https://pubmed.ncbi.nlm.nih.gov/PMC4602070/">pmcid:PMC4602070</a>
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<a target="_blank" rel="noopener" href="https://web.archive.org/web/20181030075003/https://link.springer.com/content/pdf/10.1007%2Fs00335-015-9586-7.pdf" title="fulltext PDF download" data-goatcounter-click="serp-fulltext" data-goatcounter-title="serp-fulltext">
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Viable Ednra Y129F mice feature human mandibulofacial dysostosis with alopecia (MFDA) syndrome due to the homologue mutation
<span title="2016-09-26">2016</span>
<i title="Springer Nature">
<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/2wcheulsyvd7bott7zn35dhoti" style="color: black;">Mammalian Genome</a>
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Animal models resembling human mutations are valuable tools to research the features of complex human craniofacial syndromes. This is the first report on a viable dominant mouse model carrying a non-synonymous sequence variation within the endothelin receptor type A gene (Ednra c.386A[T, p.Tyr129Phe) derived by an ENU mutagenesis program. The identical amino acid substitution was reported recently as disease causing in three individuals with the mandibulofacial dysostosis with alopecia (MFDA,
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<a target="_blank" rel="external noopener" href="https://www.ncbi.nlm.nih.gov/pubmed/27671791">pmid:27671791</a>
<a target="_blank" rel="external noopener" href="https://pubmed.ncbi.nlm.nih.gov/PMC5110705/">pmcid:PMC5110705</a>
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... IM 616367) syndrome. We performed standardized phenotyping of wild-type, heterozygous, and homozygous Ednra Y129F mice within the German Mouse Clinic. Mutant mice mimic the craniofacial phenotypes of jaw dysplasia, micrognathia, dysplastic temporomandibular joints, auricular dysmorphism, and missing of the squamosal zygomatic process as described for MFDA-affected individuals. As observed in MFDA-affected individuals, mutant Ednra Y129F mice exhibit hearing impairment in line with strong abnormalities of the ossicles and further, reduction of some lung volumetric parameters. In general, heterozygous and
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Myoscape controls cardiac calcium cycling and contractility via regulation of L-type calcium channel surface expression
<span title="2016-04-28">2016</span>
<i title="Springer Nature">
<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/a4wan6l5o5dfzn767kyz7jqevi" style="color: black;">Nature Communications</a>
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Calcium signalling plays a critical role in the pathogenesis of heart failure. Here we describe a cardiac protein named Myoscape/FAM40B/STRIP2, which directly interacts with the L-type calcium channel. Knockdown of Myoscape in cardiomyocytes decreases calcium transients associated with smaller Ca 2 þ amplitudes and a lower diastolic Ca 2 þ content. Likewise, L-type calcium channel currents are significantly diminished on Myoscape ablation, and downregulation of Myoscape significantly reduces
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... tractility of cardiomyocytes. Conversely, overexpression of Myoscape increases global Ca 2 þ transients and enhances L-type Ca 2 þ channel currents, and is sufficient to restore decreased currents in failing cardiomyocytes. In vivo, both Myoscape-depleted morphant zebrafish and Myoscape knockout (KO) mice display impairment of cardiac function progressing to advanced heart failure. Mechanistically, Myoscape-deficient mice show reduced L-type Ca 2 þ currents, cell capacity and calcium current densities as a result of diminished LTCC surface expression. Finally, Myoscape expression is reduced in hearts from patients suffering of terminal heart failure, implying a role in human disease.
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Mouse large-scale phenotyping initiatives: overview of the European Mouse Disease Clinic (EUMODIC) and of the Wellcome Trust Sanger Institute Mouse Genetics Project
<span title="2012-09-09">2012</span>
<i title="Springer Nature">
<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/2wcheulsyvd7bott7zn35dhoti" style="color: black;">Mammalian Genome</a>
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Two large-scale phenotyping efforts,
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<a target="_blank" rel="external noopener" href="https://www.ncbi.nlm.nih.gov/pubmed/22961258">pmid:22961258</a>
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A comprehensive and comparative phenotypic analysis of the collaborative founder strains identifies new and known phenotypes
<span title="2020-02-14">2020</span>
<i title="Springer Science and Business Media LLC">
<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/2wcheulsyvd7bott7zn35dhoti" style="color: black;">Mammalian Genome</a>
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The collaborative cross (CC) is a large panel of mouse-inbred lines derived from eight founder strains (NOD/ShiLtJ, NZO/HILtJ, A/J, C57BL/6J, 129S1/SvImJ, CAST/EiJ, PWK/PhJ, and WSB/EiJ). Here, we performed a comprehensive and comparative phenotyping screening to identify phenotypic differences and similarities between the eight founder strains. In total, more than 300 parameters including allergy, behavior, cardiovascular, clinical blood chemistry, dysmorphology, bone and cartilage, energy
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<a target="_blank" rel="external noopener noreferrer" href="https://doi.org/10.1007/s00335-020-09827-3">doi:10.1007/s00335-020-09827-3</a>
<a target="_blank" rel="external noopener" href="https://www.ncbi.nlm.nih.gov/pubmed/32060626">pmid:32060626</a>
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... bolism, eye and vision, immunology, lung function, neurology, nociception, and pathology were analyzed; in most traits from sixteen females and sixteen males. We identified over 270 parameters that were significantly different between strains. This study highlights the value of the founder and CC strains for phenotype-genotype associations of many genetic traits that are highly relevant to human diseases. All data described here are publicly available from the mouse phenome database for analyses and downloads.
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Innovations in phenotyping of mouse models in the German Mouse Clinic
<span title="2012-08-29">2012</span>
<i title="Springer Nature">
<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/2wcheulsyvd7bott7zn35dhoti" style="color: black;">Mammalian Genome</a>
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Under the label of the German Mouse Clinic (GMC), a concept has been developed and implemented that allows the better understanding of human diseases on the pathophysiological and molecular level. This includes better understanding of the crosstalk between different organs, pleiotropy of genes, and the systemic impact of envirotypes and drugs. In the GMC, experts from various fields of mouse genetics and physiology, in close collaboration with clinicians, work side by side under one roof. The
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<a target="_blank" rel="external noopener noreferrer" href="https://doi.org/10.1007/s00335-012-9415-1">doi:10.1007/s00335-012-9415-1</a>
<a target="_blank" rel="external noopener" href="https://www.ncbi.nlm.nih.gov/pubmed/22926221">pmid:22926221</a>
<a target="_blank" rel="external noopener" href="https://pubmed.ncbi.nlm.nih.gov/PMC3463795/">pmcid:PMC3463795</a>
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... C is an open-access platform for the scientific community by providing phenotypic analysis in bilateral collaborations ("bottom-up projects") and as a partner and driver in international large-scale biology projects ("topdown projects"). Furthermore, technology development is H. Fuchs and V. Gailus-Durner contributed equally to this work. H.
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The Role of Fibroblast Growth Factor-Binding Protein 1 in Skin Carcinogenesis and Inflammation
<span title="">2018</span>
<i title="Elsevier BV">
<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/hxva2c3v7rgxffw6x5wzadfdrm" style="color: black;">Journal of Investigative Dermatology</a>
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Fibroblast growth factor-binding protein 1 (FGFBP1, FGF-BP) is a secreted chaperone that mobilizes paracrine-acting FGFs, stored in the extracellular matrix, and presents them to their cognate receptors. FGFBP1 enhances FGF signaling including angiogenesis during cancer progression, and is upregulated in various cancers. Here we evaluated the contribution of endogenous FGFBP1 to development and homeostasis as well as to skin pathologies utilizing Fgfbp1-knockout (KO) mice. Relative to wild-type
<span class="external-identifiers">
<a target="_blank" rel="external noopener noreferrer" href="https://doi.org/10.1016/j.jid.2017.07.847">doi:10.1016/j.jid.2017.07.847</a>
<a target="_blank" rel="external noopener" href="https://www.ncbi.nlm.nih.gov/pubmed/28864076">pmid:28864076</a>
<a target="_blank" rel="external noopener" href="https://pubmed.ncbi.nlm.nih.gov/PMC5742071/">pmcid:PMC5742071</a>
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... (WT) littermates KO mice showed no gross pathologies. Still, in KO mice a significant thickening of the epidermis associated with a decreased transepidermal water loss and increased proinflammatory gene expression in the skin was detected. Also, skin carcinogen challenge by DMBA/TPA resulted in delayed and reduced papillomatosis in KO mice. This was paralleled by delayed healing of skin wounds and reduced angiogenic sprouting in subcutaneous matrigel plugs. Heterozygous GFP-knock-in mice revealed rapid induction of gene expression during papilloma induction and during wound healing. Examination of WT skin grafted onto Fgfbp1 GFP knockin reporter hosts and bone marrow transplants from the GFP reporter model into WT hosts revealed that circulating Fgfbp1-expressing cells migrate into healing wounds. We conclude that tissue-resident and circulating Fgfbp1-expressing cells modulate skin carcinogenesis and inflammation. To investigate the function of endogenous FGFBP1 we generated a knockout and a knock-in GFP-reporter mouse model, to investigate the role of FGFBP1 in development, skin homeostasis and repair and during challenge by chemical carcinogenesis. Results Generation of Fgfbp1-knockout mice The complete Fgfbp1 open-reading-frame contained in exon 2 on chromosome 5 was replaced by a floxed Fgfbp1 gene and a neo-GFP cassette, resulting in Fgfbp1 +/loxP-neo-gfp mice, which were then crossed with mice expressing cre (Fig. 1a) . The resulting mouse line expressed GFP in lieu of Fgfbp1 (Fgfbp1 +/gfp ) and served to monitor activity of the Fgfbp1 promoter. To generate Fgfbp1-knockout mice (KO) the Fgfbp1 loxP-neo-gfp mice were crossed with mice expressing the recombinase Flpase and then with cre-expressing mice ( Fig. 1b-f) . The mouse strain in this study is primarily C57Bl/6N and to a lower degree SV129N. The epidermis of KO mice is thicker and has a reduced permeability Since endogenous FGFBP1 is predominantly expressed in skin (Aigner et al. 2002) , we initially focused on the analysis of the skin phenotype in the KO animals. The epidermis of adult (2-3 months old) but not juvenile KO mice (3 weeks old) showed a twofold increased thickness (p<0.05; Fig. 2a, S1a) . In contrast, the thickness of dermis, fat and panniculus muscle were not significantly different between WT and KO (Fig. 2b) . The increased thickness in KO mice coincided with an increased proliferation index in basal keratinocytes (Fig 2c, e) . Also, ~50% of the epidermis in KO mice showed multilayered
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The First Scube3 Mutant Mouse Line with Pleiotropic Phenotypic Alterations
<span title="2016-12-07">2016</span>
<i title="The Genetics Society of America">
<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/lmrbfynd2rbtzo6uhqthfvnwci" style="color: black;">G3: Genes, Genomes, Genetics</a>
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The vertebrate Scube (Signal peptide, CUB, and EGF-like domain-containing protein) family consists of three independent members, Scube1-3, which encode secreted cell surface-associated membrane glycoproteins. Limited information about the general function of this gene family is available, and their roles during adulthood. Here, we present the first Scube3 mutant mouse line (Scube3N294K/N294K), which clearly shows phenotypic alterations by carrying a missense mutation in exon 8, and thus
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<a target="_blank" rel="external noopener noreferrer" href="https://doi.org/10.1534/g3.116.033670">doi:10.1534/g3.116.033670</a>
<a target="_blank" rel="external noopener" href="https://www.ncbi.nlm.nih.gov/pubmed/27815347">pmid:27815347</a>
<a target="_blank" rel="external noopener" href="https://pubmed.ncbi.nlm.nih.gov/PMC5144972/">pmcid:PMC5144972</a>
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... tes to our understanding of SCUBE3 functions. We performed a detailed phenotypic characterization in the German Mouse Clinic (GMC). Scube3N294K/N294K mutants showed morphological abnormalities of the skeleton, alterations of parameters relevant for bone metabolism, changes in renal function, and hearing impairments. These findings correlate with characteristics of the rare metabolic bone disorder Paget disease of bone (PDB), associated with the chromosomal region of human SCUBE3 In addition, alterations in energy metabolism, behavior, and neurological functions were detected in Scube3N294K/N294K mice. The Scube3N294K/N294K mutant mouse line may serve as a new model for further studying the effect of impaired SCUBE3 gene function.
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Mutation in the mouse histone gene Hist2h3c1 leads to degeneration of the lens vesicle and severe microphthalmia
<span title="2019-04-13">2019</span>
<i title="Elsevier BV">
<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/yjwblbd3d5eozhd724smr52rhy" style="color: black;">Experimental Eye Research</a>
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During an ENU (N-ethyl-N-nitrosourea) mutagenesis screen, we observed a dominant small-eye mutant mouse with viable homozygotes. A corresponding mutant line was established and referred to as Aey69 (abnormality of the eye #69). Comprehensive phenotyping of the homozygous Aey69 mutants in the German Mouse Clinic revealed only a subset of statistically significant alterations between wild types and homozygous mutants. The mutation causes microphthalmia without a lens but with retinal
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<a target="_blank" rel="external noopener noreferrer" href="https://doi.org/10.1016/j.exer.2019.03.024">doi:10.1016/j.exer.2019.03.024</a>
<a target="_blank" rel="external noopener" href="https://www.ncbi.nlm.nih.gov/pubmed/30991053">pmid:30991053</a>
<a target="_blank" rel="external noopener" href="https://pubmed.ncbi.nlm.nih.gov/PMC6876282/">pmcid:PMC6876282</a>
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... ation. Linkage was demonstrated to mouse chromosome 3 between the markers D3Mit188 and D3Mit11. Sequencing revealed a 358 A-> C mutation (Ile120Leu) in the Hist2h3c1 gene and a 71 T-> C (Val24Ala) mutation in the Gja8 gene. Detailed analysis of eye development in the homozygous mutant mice documented a perturbed lens development starting from the lens vesicle stage including decreasing expression of crystallins as well as of lens-specific transcription factors like PITX3 and FOXE3. In contrast, we observed an early expression of retinal progenitor cells characterized by several markers including BRN3 (retinal ganglion cells) and OTX2 (cone photoreceptors). The changes in the retina at the early embryonic stages of E11.5-E15.5 happen in parallel with apoptotic processes in the lens at the respective stages. The excessive retinal hyperproliferation is characterized by an increased level of Ki67. The hyperproliferation, however, does not disrupt the differentiation and appearance of the principal retinal cell types at postnatal stages, even if the overgrowing retina covers finally the entire bulbus of the eye. Morpholino-mediated knock-down of the hist2h3ca1 gene in zebrafish leads to a specific perturbation of lens development. When injected into zebrafish zygotes, only the mutant mouse mRNA leads to severe malformations, ranging from cyclopia to severe microphthalmia. The wild-type Hist2h3c1 mRNA can rescue the morpholino-induced defects corroborating its specific function in lens development. Based upon these data, it is concluded that the ocular function of the Hist2h3c1 gene (encoding a canonical H3.2 variant) is conserved throughout evolution. Moreover, the data highlight also the importance of Hist2h3c1 in the coordinated formation of lens and retina during eye development.
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Analysis of mammalian gene function through broad-based phenotypic screens across a consortium of mouse clinics
<span title="2015-07-27">2015</span>
<i title="Springer Nature">
<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/ndd3azjmwfh45iqb6bvdfttaf4" style="color: black;">Nature Genetics</a>
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The function of the majority of genes in the mouse and human genomes remains unknown. The mouse ES cell knockout resource provides a basis for characterisation of relationships between gene and phenotype. The EUMODIC consortium developed and validated robust methodologies for broad-based phenotyping of knockouts through a pipeline comprising 20 disease-orientated platforms. We developed novel statistical methods for pipeline design and data analysis aimed at detecting reproducible phenotypes
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<a target="_blank" rel="external noopener noreferrer" href="https://doi.org/10.1038/ng.3360">doi:10.1038/ng.3360</a>
<a target="_blank" rel="external noopener" href="https://www.ncbi.nlm.nih.gov/pubmed/26214591">pmid:26214591</a>
<a target="_blank" rel="external noopener" href="https://pubmed.ncbi.nlm.nih.gov/PMC4564951/">pmcid:PMC4564951</a>
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... h high power. We acquired phenotype data from 449 mutant alleles, representing 320 unique genes, of which half had no prior functional annotation. We captured data from over 27,000 mice finding that 83% of the mutant lines are phenodeviant, with 65% demonstrating pleiotropy. Surprisingly, we found significant differences in phenotype annotation according to zygosity. Novel phenotypes were uncovered for many genes with unknown function providing a powerful basis for hypothesis generation and further investigation in diverse systems. A statistical power analysis was performed to quantify the mutant-genotype standardized effect size, d, that would be detectable under a variety of experimental workflows and analysis methods, where is the absolute difference between de Angelis et al.
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Prevalence of sexual dimorphism in mammalian phenotypic traits
<span title="2017-06-26">2017</span>
<i title="Springer Nature">
<a target="_blank" rel="noopener" href="https://fatcat.wiki/container/a4wan6l5o5dfzn767kyz7jqevi" style="color: black;">Nature Communications</a>
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