scholarly journals Bone microstructure and its associated genetic variability in 12 inbred mouse strains: μCT study and in silico genome scan

Bone ◽  
2008 ◽  
Vol 42 (2) ◽  
pp. 439-451 ◽  
Author(s):  
Ilya Sabsovich ◽  
J. David Clark ◽  
Guochun Liao ◽  
Gary Peltz ◽  
Derek P. Lindsey ◽  
...  
Keyword(s):  
Genetic Variability ◽  
In Silico ◽  
Inbred Mouse ◽  
Genome Scan ◽  
Bone Microstructure ◽  
Mouse Strains ◽  
Inbred Mouse Strains

scholarly journals In silico candidate variant and gene identification using inbred mouse strains

PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e11017
Author(s):  
Matthias Munz ◽  
Mohammad Khodaygani ◽  
Zouhair Aherrahrou ◽  
Hauke Busch ◽  
Inken Wohlers
Keyword(s):  
Fine Mapping ◽  
In Silico ◽  
Inbred Mice ◽  
Inbred Mouse ◽  
Gene Identification ◽  
Mouse Strains ◽  
Genotype Data ◽  
Inbred Mouse Strains ◽  
Phenotypic Data ◽  
Genome Wide

Mice are the most widely used animal model to study genotype to phenotype relationships. Inbred mice are genetically identical, which eliminates genetic heterogeneity and makes them particularly useful for genetic studies. Many different strains have been bred over decades and a vast amount of phenotypic data has been generated. In addition, recently whole genome sequencing-based genome-wide genotype data for many widely used inbred strains has been released. Here, we present an approach for in silico fine-mapping that uses genotypic data of 37 inbred mouse strains together with phenotypic data provided by the user to propose candidate variants and genes for the phenotype under study. Public genome-wide genotype data covering more than 74 million variant sites is queried efficiently in real-time to provide those variants that are compatible with the observed phenotype differences between strains. Variants can be filtered by molecular consequences and by corresponding molecular impact. Candidate gene lists can be generated from variant lists on the fly. Fine-mapping together with annotation or filtering of results is provided in a Bioconductor package called MouseFM. In order to characterize candidate variant lists under various settings, MouseFM was applied to two expression data sets across 20 inbred mouse strains, one from neutrophils and one from CD4+ T cells. Fine-mapping was assessed for about 10,000 genes, respectively, and identified candidate variants and haplotypes for many expression quantitative trait loci (eQTLs) reported previously based on these data. For albinism, MouseFM reports only one variant allele of moderate or high molecular impact that only albino mice share: a missense variant in the Tyr gene, reported previously to be causal for this phenotype. Performing in silico fine-mapping for interfrontal bone formation in mice using four strains with and five strains without interfrontal bone results in 12 genes. Of these, three are related to skull shaping abnormality. Finally performing fine-mapping for dystrophic cardiac calcification by comparing 9 strains showing the phenotype with eight strains lacking it, we identify only one moderate impact variant in the known causal gene Abcc6. In summary, this illustrates the benefit of using MouseFM for candidate variant and gene identification.

scholarly journals In silico candidate variant and gene identification using inbred mouse strains

2020 ◽  
Author(s):  
Matthias Munz ◽  
Mohammad Khodaygani ◽  
Zouhair Aherrahrou ◽  
Hauke Busch ◽  
Inken Wohlers
Keyword(s):  
Fine Mapping ◽  
In Silico ◽  
Inbred Mice ◽  
Inbred Mouse ◽  
Gene Identification ◽  
Mouse Strains ◽  
Genotype Data ◽  
Inbred Mouse Strains ◽  
Phenotypic Data ◽  
Genome Wide

ABSTRACTMice are the most widely used animal model to study genotype to phenotype relationships. Inbred mice are genetically identical, which eliminates genetic heterogeneity and makes them particularly useful for genetic studies. Many different strains have been bred over decades and a vast amount of phenotypic data has been generated. In addition, recently whole genome sequencing-based genome-wide genotype data for many widely used inbred strains has been released. Here, we present an approach for in silico fine-mapping that uses genotypic data of 37 inbred mouse strains together with phenotypic data provided by the user to propose candidate variants and genes for the phenotype under study. Public genome-wide genotype data covering more than 74 million variant sites is queried efficiently in real-time to provide those variants that are compatible with the observed phenotype differences between strains. Variants can be filtered by molecular consequences and by corresponding molecular impact. Candidate gene lists can be generated from variant lists on the fly. Fine-mapping together with annotation or filtering of results is provided in a Bioconductor package called MouseFM. In order to characterize candidate variant lists under various settings, MouseFM was applied to two expression data sets across 20 inbred mouse strains, one from neutrophils and one from CD4+ T cells. Fine-mapping was assessed for about 10,000 genes, respectively, and identified candidate variants and haplotypes for many expression quantitative trait loci (eQTLs) reported previously based on these data. For albinism, MouseFM reports only one variant allele of moderate or high molecular impact that only albino mice share: a missense variant in the Tyr gene, reported previously to be causal for this phenotype. Performing in silico fine-mapping for interfrontal bone formation in mice using four strains with and five strains without interfrontal bone results in 12 genes. Of these, three are related to skull shaping abnormality. Finally performing fine-mapping for dystrophic cardiac calcification by comparing 9 strains showing the phenotype with 8 strains lacking it, we identify only one moderate impact variant in the known causal gene Abcc6. In summary, this illustrates the benefit of using MouseFM for candidate variant and gene identification.

scholarly journals THE Ah PHENOTYPE. SURVEY OF FORTY-EIGHT RAT STRAINS AND TWENTY INBRED MOUSE STRAINS

Genetics ◽  
1982 ◽  
Vol 100 (1) ◽  
pp. 79-87
Author(s):  
Daniel W Nebert ◽  
Nancy M Jensen ◽  
Hisashi Shinozuka ◽  
Heinz W Kunz ◽  
Thomas J Gill
Keyword(s):  
Specific Activity ◽  
Inbred Mouse ◽  
Inbred Mouse Strain ◽  
Mouse Strains ◽  
Ah Receptor ◽  
Inbred Mouse Strains ◽  
Sprague Dawley ◽  
Rat Strains ◽  
Specific Activities ◽  
Inbred Rat

ABSTRACT Forty-four inbred and four randombred rat strains and 20 inbred mouse strains were examined for their Ah phenotype by determining the induction of liver microsomal aryl hydrocarbon (benzo[a]pyrene) hydroxylase activity (EC 1.14.14.1) by intraperitoneal treatment with either β-naphthoflavone or 3-methylcholanthrene. All 48 rat strains were found to be Ah-responsive. The maximally induced hydroxylase specific activities of the ALB/Pit, MNR/Pit, MR/Pit, SHR/Pit, and Sprague-Dawley strains were of the same order of magnitude as the basal hydroxylase specific activities of the ACI/Pit, F344/Pit, OKA/Pit, and MNR/N strains. Six of the 20 mouse strains were Ah-nonresponsive (i.e. lacking the normal induction response and presumably lacking detectable amounts of the Ah receptor). The basal hydroxylase specific activities of the BDL/N, NFS/N, STAR/N, and ST/JN mouse strains were more than twice as high as the maximally induced hydroxylase specific activity of the CBA/HT strain.——To date, 24 Ah-nonresponsive mouse strains have been identified, out of a total of 68 known to have been characterized. The reasons for not finding a single Ah-nonresponsive inbred rat strain—as compared with about one Ah-nonresponsive inbred mouse strain found for every three examined—remain unknown.

scholarly journals Relationship between phospholipid transfer protein activity and HDL level and size among inbred mouse strains

1999 ◽  
Vol 40 (2) ◽  
pp. 295-301 ◽  
Author(s):  
John J. Albers ◽  
Wendy Pitman ◽  
Gertrud Wolfbauer ◽  
Marian C. Cheung ◽  
Hal Kennedy ◽  
...  
Keyword(s):  
Inbred Mouse ◽  
Mouse Strains ◽  
Phospholipid Transfer Protein ◽  
Inbred Mouse Strains ◽  
Protein Activity ◽  
Transfer Protein ◽  
Phospholipid Transfer
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