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Journal articles on the topic 'Mice – Genetics'

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Published: 4 June 2021

Last updated: 20 February 2023

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1

Nilsson, Annika I., Elisabeth Kugelberg, Otto G. Berg, and Dan I. Andersson. "Experimental Adaptation ofSalmonella typhimuriumto Mice." Genetics 168, no. 3 (November 2004): 1119–30. http://dx.doi.org/10.1534/genetics.104.030304.

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2

Cook, Donald N., Gregory S. Whitehead, Lauranell H. Burch, Katherine G. Berman, Zareen Kapadia, Christine Wohlford-Lenane, and David A. Schwartz. "Spontaneous Mutations in Recombinant Inbred Mice: Mutant Toll-like Receptor 4 (Tlr4) in BXD29 Mice." Genetics 172, no. 3 (December 1, 2005): 1751–55. http://dx.doi.org/10.1534/genetics.105.042820.

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3

Jasny, B. "MOLECULAR GENETICS: Making Mito-Mice." Science 290, no. 5492 (October 27, 2000): 673a—673. http://dx.doi.org/10.1126/science.290.5492.673a.

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4

Kono, Dwight H., and Argyrios N. Theofilopoulos. "Genetics of SLE in mice." Springer Seminars in Immunopathology 28, no. 2 (September 14, 2006): 83–96. http://dx.doi.org/10.1007/s00281-006-0030-7.

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5

Landel, C. P., S. Chen, and G. A. Evans. "Reverse Genetics Using Transgenic Mice." Annual Review of Physiology 52, no. 1 (October 1990): 841–51. http://dx.doi.org/10.1146/annurev.ph.52.030190.004205.

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6

Legarra, Andrés, Christèle Robert-Granié, Eduardo Manfredi, and Jean-Michel Elsen. "Performance of Genomic Selection in Mice." Genetics 180, no. 1 (August 30, 2008): 611–18. http://dx.doi.org/10.1534/genetics.108.088575.

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7

Clarke, Angus. "Genetic imprinting in clinical genetics." Development 108, Supplement (April 1, 1990): 131–39. http://dx.doi.org/10.1242/dev.108.supplement.131.

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Genetic, and indeed genomic, imprinting does occur in humans. This is manifest at the level of the genome, the individual chromosome, subchromosomal region or fragile site, or the single locus. The best evidence at the single gene level comes from a consideration of familial tumour syndromes. Chromosomal imprinting effects are revealed when uniparental disomy occurs, as in the Prader-Willi syndrome and doubtless other sporadic, congenital anomaly syndromes. Genomic imprinting is manifest in the developmental defects of hydatidiform mole, teratoma and triploidy. Fragile (X) mental retardation shows an unusual pattern of inheritance, and imprinting can account for these effects. Future work in clinical genetics may identify congenital anomalies and growth disorders caused by imprinting: the identification of imprinting effects for specific chromosomal regions in mice will allow the examination of the homologous chromosomal region in humans.

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8

Lee, G. H., L. M. Bennett, R. A. Carabeo, and N. R. Drinkwater. "Identification of hepatocarcinogen-resistance genes in DBA/2 mice." Genetics 139, no. 1 (January 1, 1995): 387–95. http://dx.doi.org/10.1093/genetics/139.1.387.

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Abstract Male DBA/2J mice are approximately 20-fold more susceptible than male C57BL/6J mice to hepatocarcinogenesis induced by perinatal treatment with N,N-diethylnitrosamine (DEN). In order to elucidate the genetic control of hepatocarcinogenesis in DBA/2J mice, male BXD recombinant inbred, D2B6F1 x B6 backcross, and D2B6F2 intercross mice were treated at 12 days of age with DEN and liver tumors were enumerated at 32 weeks. Interestingly, the distribution of mean tumor multiplicities among BXD recombinant inbred strains indicated that hepatocarcinogen-sensitive DBA/2 mice carry multiple genes with opposing effects on the susceptibility to liver tumor induction. By analyzing D2B6F1 x B6 backcross and D2B6F2 intercross mice for their liver tumor multiplicity phenotypes and for their genotypes at simple sequence repeat marker loci, we mapped two resistance genes carried by DBA/2J mice, designated Hcr1 and -2, to chromosomes 4 and 10, respectively. Hcr1 and Hcr2 resolved the genetic variance in the backcross population well, indicating that these resistance loci are the major determinants of the variance in the backcross population. Although our collection of 100 simple sequence repeat markers allowed linkage analysis for approximately 95% of the genome, we failed to map any sensitivity alleles for DBA/2J mice. Thus, it is likely that the susceptibility of DBA/2J mice is the consequence of the combined effects of multiple sensitivity loci.

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9

Gelman, R., A. Watson, E. Yunis, and R. M. Williams. "Genetics of survival in mice: subregions of the major histocompatibility complex." Genetics 125, no. 1 (May 1, 1990): 167–74. http://dx.doi.org/10.1093/genetics/125.1.167.

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Abstract In this study of murine survival, 422 F1 hybrids between DBA/2J (D2) female mice and C57BL/10 (B10) background H-2 congenic male mice (11 strains), 88 F1 hybrids between B10 female mice and B10 background H-2 congenic male mice (3 strains), and 532 control mice from the 11 parental B10 background H-2 congenic mice were bred over a period of 2 yr. Toward the end of the breeding period there was documentation of Sendai infection in the mouse rooms. All analyses were done separately for the two sexes. Although it did not appear that an unusually high number of mice died during the time the colony was infected with Sendai, there was a highly significant tendency for mice who were younger at the time of the Sendai infection to have shorter survival than mice who were older at that time point. The effect of birth date on survival was approximately as significant as the effect of strain on survival. Hence all analyses of genetic effects on survival were either done within subsets of mice born in the same quarter of a particular year or else included date of birth variables in survival models. Of the 18 possible comparisons of pairs of strains which overlapped in birth dates and differed only in the D end of H-2, five were associated with highly significant survival differences. Of the 11 pairs of strains which overlapped in birth date and differed only in the K end of H-2, none was associated with significant survival differences.(ABSTRACT TRUNCATED AT 250 WORDS)

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10

Roper, Randall J., Heidi K. St. John, Jessica Philip, Ann Lawler, and Roger H. Reeves. "Perinatal Loss of Ts65Dn Down Syndrome Mice." Genetics 172, no. 1 (September 19, 2005): 437–43. http://dx.doi.org/10.1534/genetics.105.050898.

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11

Crow, James F. "C. C. Little, Cancer and Inbred Mice." Genetics 161, no. 4 (August 1, 2002): 1357–61. http://dx.doi.org/10.1093/genetics/161.4.1357.

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12

Salcedo, Tovah, Armando Geraldes, and Michael W. Nachman. "Nucleotide Variation in Wild and Inbred Mice." Genetics 177, no. 4 (December 2007): 2277–91. http://dx.doi.org/10.1534/genetics.107.079988.

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13

Ginsburg, David. "Genetic Modifiers of Thrombosis in Mice." Blood 114, no. 22 (November 20, 2009): SCI—44—SCI—44. http://dx.doi.org/10.1182/blood.v114.22.sci-44.sci-44.

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Abstract Abstract SCI-44 The genetic factors responsible for the highly variable clinical course of inherited bleeding disorders including von Willebrand disease and hemophilia are largely unknown. Similar factors are also likely to contribute to the variability of common thrombotic disorders, including factor V Leiden. Studies by our lab over the past 10 years have used the power of mouse genetics to identify genes contributing to this variability (referred to as ‘modifier‘ genes). By performing genetic crosses between inbred strains of mice with elevated plasma levels of von Willebrand Factor (VWF) and other strains with low levels, we have mapped a total of 6 genetic factors contributing to the control of murine plasma VWF levels. Similar studies in ADAMTS13-deficient mice are in progress aimed at characterizing genes modifying susceptibility thrombotic thrombocytopenic purpura. We have also conducted large scale mutagenesis studies in the mouse in an effort to identify larger numbers of genes contributing to thrombosis risk in the setting of Factor V Leiden, and most recently are extending this approach to similar genetic screens in zebrafish. Finally, recent advances in human genetics are expanding the potential opportunities for directly identifying bleeding and thrombosis modifier genes in humans. Disclosures No relevant conflicts of interest to declare.

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14

Nakai, Ayaka, Tomoyuki Fujiyama, Nanae Nagata, Mitsuaki Kashiwagi, Aya Ikkyu, Marina Takagi, Chika Tatsuzawa, et al. "Sleep Architecture in Mice Is Shaped by the Transcription Factor AP-2β." Genetics 216, no. 3 (September 2, 2020): 753–64. http://dx.doi.org/10.1534/genetics.120.303435.

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The molecular mechanism regulating sleep largely remains to be elucidated. In humans, families that carry mutations in TFAP2B, which encodes the transcription factor AP-2β, self-reported sleep abnormalities such as short-sleep and parasomnia. Notably, AP-2 transcription factors play essential roles in sleep regulation in the nematode Caenorhabditis elegans and the fruit fly Drosophila melanogaster. Thus, AP-2 transcription factors might have a conserved role in sleep regulation across the animal phyla. However, direct evidence supporting the involvement of TFAP2B in mammalian sleep was lacking. In this study, by using the CRISPR/Cas9 technology, we generated two Tfap2b mutant mouse strains, Tfap2bK144 and Tfap2bK145, each harboring a single-nucleotide mutation within the introns of Tfap2b mimicking the mutations in two human kindreds that self-reported sleep abnormalities. The effects of these mutations were compared with those of a Tfap2b knockout allele (Tfap2b–). The protein expression level of TFAP2B in the embryonic brain was reduced to about half in Tfap2b+/− mice and was further reduced in Tfap2b−/− mice. By contrast, the protein expression level was normal in Tfap2bK145/+ mice but was reduced in Tfap2bK145/K145 mice to a similar extent as Tfap2b−/− mice. Tfap2bK144/+ and Tfap2bK144/K144 showed normal protein expression levels. Tfap2b+/− female mice showed increased wakefulness time and decreased nonrapid eye movement sleep (NREMS) time. By contrast, Tfap2bK145/+ female mice showed an apparently normal amount of sleep but instead exhibited fragmented NREMS, whereas Tfap2bK144/+ male mice showed reduced NREMS time specifically in the dark phase. Finally, in the adult brain, Tfap2b-LacZ expression was detected in the superior colliculus, locus coeruleus, cerebellum, and the nucleus of solitary tract. These findings provide direct evidence that TFAP2B influences NREMS amounts in mice and also show that different mutations in Tfap2b can lead to diverse effects on sleep architecture.

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15

Lam, Man-Yee Josephine, Kirsten K. Youngren, and Joseph H. Nadeau. "Enhancers and Suppressors of Testicular Cancer Susceptibility in Single- and Double-Mutant Mice." Genetics 166, no. 2 (February 1, 2004): 925–33. http://dx.doi.org/10.1093/genetics/166.2.925.

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Abstract Susceptibility to spontaneous testicular germ cell tumors (TGCTs), a common cancer affecting young men, shows unusual genetic complexity. Despite remarkable progress in the genetics analysis of susceptibility to many cancers, TGCT susceptibility genes have not yet been identified. Various mutations that are inherited as Mendelian traits in laboratory mice affect susceptibility to spontaneous TGCTs on the 129/Sv inbred genetic background. We compared the frequency of spontaneous TGCTs in single- and double-mutant mice to identify combinations that show evidence of enhancer or suppressor effects. The lower-than-expected TGCT frequencies in mice with partial deficiencies of TRP53 and MGF-SLJ and in 129.MOLF-Chr19 (M19) consomic mice that were heterozygous for the Ay mutation suggest that either these genes complement each other to restore normal functionality in TGCT stem cells or together these genes activate mechanisms that suppress incipient TGCTs. By contrast, the higher-than-expected TGCT frequencies in Mgf Sl-J-M19 compound heterozygous mice suggest that these mutations exacerbate each other’s effects. Together, these results provide clues to the genetic and molecular basis for susceptibility to TGCTs in mice and perhaps in humans.

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16

Panthier, J. J., J. L. Guénet, H. Condamine, and F. Jacob. "Evidence for mitotic recombination in Wei/+ heterozygous mice." Genetics 125, no. 1 (May 1, 1990): 175–82. http://dx.doi.org/10.1093/genetics/125.1.175.

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Abstract A number of alleles at coat color loci of the house mouse give rise to areas of wild-type pigmentation on the coats of otherwise mutant animals. Such unstable alleles include both recessive and dominant mutations. Among the latter are several alleles at the W locus. In this report, phenotypic reversions of the Wei allele at the W locus were studied Mice heterozygous in repulsion for both Wei and buff (bf) [i.e. Wei+/+bf] were examined for the occurrence of phenotypic reversion events. Buff (bf) is a recessive mutation, which lies 21 cM from W on the telomeric side of chromosome 5 and is responsible for the khaki colored coat of nonagouti buff homozygotes (a/a; bf/bf). Two kinds of fully pigmented reversion spots were recovered on the coats of a/a; Wei+/+bf mice: either solid black or khaki colored. Furthermore phenotypic reversions of Wei/+ were enhanced significantly following X-irradiation of 9.25-day-old Wei/+ embryos (P less than 0.04). These observations are consistent with the suggestion of a role for mitotic recombination in the origin of these phenotypic reversions. In addition these results rise the intriguing possibility that some W mutations may enhance mitotic recombination in the house mouse.

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17

Gunn, T. M., T. Inui, K. Kitada, S. Ito, K. Wakamatsu, L. He, D. M. Bouley, T. Serikawa, and G. S. Barsh. "Molecular and Phenotypic Analysis of Attractin Mutant Mice." Genetics 158, no. 4 (August 1, 2001): 1683–95. http://dx.doi.org/10.1093/genetics/158.4.1683.

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Abstract Mutations of the mouse Attractin (Atrn; formerly mahogany) gene were originally recognized because they suppress Agouti pigment type switching. More recently, effects independent of Agouti have been recognized: mice homozygous for the Atrnmg-3J allele are resistant to diet-induced obesity and also develop abnormal myelination and vacuolation in the central nervous system. To better understand the pathophysiology and relationship of these pleiotropic effects, we further characterized the molecular abnormalities responsible for two additional Atrn alleles, Atrnmg and Atrnmg-L, and examined in parallel the phenotypes of homozygous and compound heterozygous animals. We find that the three alleles have similar effects on pigmentation and neurodegeneration, with a relative severity of Atrnmg-3J > Atrnmg > Atrnmg-L, which also corresponds to the effects of the three alleles on levels of normal Atrn mRNA. Animals homozygous for Atrnmg-3J or Atrnmg, but not Atrnmg-L, show reduced body weight, reduced adiposity, and increased locomotor activity, all in the presence of normal food intake. These results confirm that the mechanism responsible for the neuropathological alteration is a loss—rather than gain—of function, indicate that abnormal body weight in Atrn mutant mice is caused by a central process leading to increased energy expenditure, and demonstrate that pigmentation is more sensitive to levels of Atrn mRNA than are nonpigmentary phenotypes.

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18

Panda, Sudeepta Kumar, Benedikt Wefers, Oskar Ortiz, Thomas Floss, Bettina Schmid, Christian Haass, Wolfgang Wurst, and Ralf Kühn. "Highly Efficient Targeted Mutagenesis in Mice Using TALENs." Genetics 195, no. 3 (August 26, 2013): 703–13. http://dx.doi.org/10.1534/genetics.113.156570.

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19

Kousathanas, Athanasios, Daniel L. Halligan, and Peter D. Keightley. "Faster-X Adaptive Protein Evolution in House Mice." Genetics 196, no. 4 (December 20, 2013): 1131–43. http://dx.doi.org/10.1534/genetics.113.158246.

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20

Barrington, William T., Phillip Wulfridge, Ann E. Wells, Carolina Mantilla Rojas, Selene Y. F. Howe, Amie Perry, Kunjie Hua, et al. "Improving Metabolic Health Through Precision Dietetics in Mice." Genetics 208, no. 1 (November 20, 2017): 399–417. http://dx.doi.org/10.1534/genetics.117.300536.

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21

Morgan, Andrew P., Timothy A. Bell, James J. Crowley, and Fernando Pardo-Manuel de Villena. "Instability of the Pseudoautosomal Boundary in House Mice." Genetics 212, no. 2 (April 26, 2019): 469–87. http://dx.doi.org/10.1534/genetics.119.302232.

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22

Cui, Xiangqin, Jason Affourtit, Keith R. Shockley, Yong Woo, and Gary A. Churchill. "Inheritance Patterns of Transcript Levels in F1Hybrid Mice." Genetics 174, no. 2 (August 3, 2006): 627–37. http://dx.doi.org/10.1534/genetics.106.060251.

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23

Johnson, Britt A., Brian S. Cole, Eldon E. Geisert, Sakae Ikeda, and Akihiro Ikeda. "Tyrosinase Is the Modifier of Retinoschisis in Mice." Genetics 186, no. 4 (September 27, 2010): 1337–44. http://dx.doi.org/10.1534/genetics.110.120840.

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24

Hammer, Michael F., and Allan C. Wilson. "Regulatory and Structural Genes for Lysozymes of Mice." Genetics 115, no. 3 (March 1, 1987): 521–33. http://dx.doi.org/10.1093/genetics/115.3.521.

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ABSTRACT The molecular and genetic basis of large differences in the concentration of P lysozyme in the small intestine has been investigated by crossing inbred strains of two species of house mouse (genus Mus). The concentration of P in domesticus is about 130-fold higher than in castaneus . An autosomal genetic element determining the concentration of P has been identified and named the P lysozyme regulator, Lzp-r . The level of P in interspecific hybrids (domesticus x castaneus) as well as in certain classes of backcross progeny is intermediate relative to parental levels, which shows that the two alleles of Lzp-r are inherited additively. There are two forms of P lysozyme in the intestine of the interspecific hybrid-one having the heat stability of domesticus P, the other being more stable and presumably the product of the castaneus P locus. These two forms occur in equal amounts, and it appears that Lzp-r acts in trans. The linkage of Lzp-r to three structural genes (Lzp-s, Lzm-s1, and Lzm-s2), one specifying P lysozyme and two specifying M lysozymes, was shown by electrophoretic analysis of backcrosses involving domesticus and castaneus and also domesticus and spretus . The role of regulatory mutations in evolution is discussed in light of these results.

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25

Davenport, R. J. "GENETICS: Faster Maps Mean Fewer Mice." Science 292, no. 5523 (June 8, 2001): 1814–15. http://dx.doi.org/10.1126/science.292.5523.1814.

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26

Fitch, K. R. "Genetics of dark skin in mice." Genes & Development 17, no. 2 (January 15, 2003): 214–28. http://dx.doi.org/10.1101/gad.1023703.

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27

Yunis, E. J., and M. Salazar. "Genetics of life span in mice." Genetica 91, no. 1-3 (February 1993): 211–23. http://dx.doi.org/10.1007/bf01435999.

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28

Whitney, Glayde, and David B. Harder. "Genetics of bitter perception in mice." Physiology & Behavior 56, no. 6 (December 1994): 1141–47. http://dx.doi.org/10.1016/0031-9384(94)90358-1.

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29

Beutler, Bruce, Xin Du, and Yu Xia. "Precis on forward genetics in mice." Nature Immunology 8, no. 7 (July 2007): 659–64. http://dx.doi.org/10.1038/ni0707-659.

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30

Allen, K. M., and T. N. Seyfried. "Genetic analysis of nucleotide triphosphatase activity in the mouse brain." Genetics 137, no. 1 (May 1, 1994): 257–65. http://dx.doi.org/10.1093/genetics/137.1.257.

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Abstract A Ca(2+)- or Mg(2+)-stimulated ecto-ATPase is thought to regulate the hydrolysis of extracellular ATP in nervous tissues. The hydrolysis of nucleotide triphosphates (NTPs) was analyzed in brain microsomal fractions from crosses of DBA/2J (D2) and C57BL/6J (B6) mice. The nucleotide triphosphatase (NTPase) activity was significantly reduced in D2 mice as compared to B6 mice, and B6D2F1 hybrids had activities intermediate to the parentals. A significant positive correlation was found between the hydrolysis of four NTPs (ATP, CTP, GTP and UTP) in 24 B6 x D2 (BXD) recombinant inbred (RI) strains of mice and in 80 B6D2F1 x D2 backcross mice. The RI strains and backcross mice fell into two distinct groups with respect to the NTPase activity. Linkage of NTPase activity was suggested with the chromosome 2 markers, D2Mit6 and Ass-1, in the RI strains, and was confirmed by analysis of other markers in the backcross population. These data suggest that the Ca(2+)- or Mg(2+)-stimulated hydrolysis of NTPs, designated Ntp, is regulated by a single gene located on proximal chromosome 2. Although an association was observed previously between Ca(2+)-ATPase activity and susceptibility to audiogenic seizures (AGS), no significant association was observed for the expression of Ntp and AGS susceptibility.

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31

Chebib, Jobran, Benjamin C. Jackson, Eugenio López-Cortegano, Diethard Tautz, and Peter D. Keightley. "Inbred lab mice are not isogenic: genetic variation within inbred strains used to infer the mutation rate per nucleotide site." Heredity 126, no. 1 (August 31, 2020): 107–16. http://dx.doi.org/10.1038/s41437-020-00361-1.

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AbstractFor over a century, inbred mice have been used in many areas of genetics research to gain insight into the genetic variation underlying traits of interest. The generalizability of any genetic research study in inbred mice is dependent upon all individual mice being genetically identical, which in turn is dependent on the breeding designs of companies that supply inbred mice to researchers. Here, we compare whole-genome sequences from individuals of four commonly used inbred strains that were procured from either the colony nucleus or from a production colony (which can be as many as ten generations removed from the nucleus) of a large commercial breeder, in order to investigate the extent and nature of genetic variation within and between individuals. We found that individuals within strains are not isogenic, and there are differences in the levels of genetic variation that are explained by differences in the genetic distance from the colony nucleus. In addition, we employ a novel approach to mutation rate estimation based on the observed genetic variation and the expected site frequency spectrum at equilibrium, given a fully inbred breeding design. We find that it provides a reasonable per nucleotide mutation rate estimate when mice come from the colony nucleus (~7.9 × 10−9 in C3H/HeN), but substantially inflated estimates when mice come from production colonies.

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32

D'Surney, S. J., and R. A. Popp. "Oxygen association-dissociation and stability analysis on mouse hemoglobins with mutant alpha- and beta-globins." Genetics 132, no. 2 (October 1, 1992): 545–51. http://dx.doi.org/10.1093/genetics/132.2.545.

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Abstract Oxygen association-dissociation and hemoglobin stability analysis were performed on mouse hemoglobins with amino acid substitutions in an alpha-globin (alpha 89, His to Leu) and a beta-globin (beta 59, Lys to Ile). The variant alpha-globin, designated chain 5m in the Hbag2 haplotype, had an high oxygen affinity and was stable. The variant beta-globin, (beta s2) of the Hbbs2 haplotype, also had an elevated oxygen affinity and in addition was moderately unstable in 19% isopropanol. Hemoglobins from the expected nine (Hbag2/Hbag2;Hbbs/Hbbs x Hbaa/Hbaa;Hbbs2/Hbbs2) F2 genotypes can be grouped into five classes of P50 values characterized by strict additivity and dependency on mutant globin gene dosage; physiologically, both globin variants gave indistinguishable effects on oxygen affinity. The hemoglobin of normal mice (Hbaa/Hbaa;Hbbs/Hbbs) had a P50 = 40 mm Hg and the hemoglobin of Hbag2/Hbag2;Hbbs2/Hbbs2 F2 mice had a P50 = 25 mm Hg (human P50 = 26 mm Hg). Peripheral blood from Hbag2/Hbag2;Hbbs/Hbbs, Hbaa/Hbaa;Hbbs2/Hbbs2 and Hbag2/Hbag2;Hbbs2/Hbbs2 mice exhibited normal hematological values except for a slightly higher hematocrit for Hbag2/Hbag2;Hbbs/Hbbs and Hbag2/Hbag2;Hbbs2/Hbbs2 mice, slightly elevated red cell counts for mice of the three mutant genotypes, and significantly lower values for the mean corpuscular volume and mean corpuscular hemoglobin for Hbag2/Hbag2;Hbbs2/Hbbs2 mice.

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33

Carlson, Corey M., Adam J. Dupuy, Sabine Fritz, Kevin J. Roberg-Perez, Colin F. Fletcher, and David A. Largaespada. "Transposon Mutagenesis of the Mouse Germline." Genetics 165, no. 1 (September 1, 2003): 243–56. http://dx.doi.org/10.1093/genetics/165.1.243.

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Abstract Sleeping Beauty is a synthetic “cut-and-paste” transposon of the Tc1/mariner class. The Sleeping Beauty transposase (SB) was constructed on the basis of a consensus sequence obtained from an alignment of 12 remnant elements cloned from the genomes of eight different fish species. Transposition of Sleeping Beauty elements has been observed in cultured cells, hepatocytes of adult mice, one-cell mouse embryos, and the germline of mice. SB has potential as a random germline insertional mutagen useful for in vivo gene trapping in mice. Previous work in our lab has demonstrated transposition in the male germline of mice and transmission of novel inserted transposons in offspring. To determine sequence preferences and mutagenicity of SB-mediated transposition, we cloned and analyzed 44 gene-trap transposon insertion sites from a panel of 30 mice. The distribution and sequence content flanking these cloned insertion sites was compared to 44 mock insertion sites randomly selected from the genome. We find that germline SB transposon insertion sites are AT-rich and the sequence ANNTANNT is favored compared to other TA dinucleotides. Local transposition occurs with insertions closely linked to the donor site roughly one-third of the time. We find that ∼27% of the transposon insertions are in transcription units. Finally, we characterize an embryonic lethal mutation caused by endogenous splicing disruption in mice carrying a particular intron-inserted gene-trap transposon.

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34

Prager, Ellen M., Cristián Orrego, and Richard D. Sage. "Genetic Variation and Phylogeography of Central Asian and Other House Mice, Including a Major New Mitochondrial Lineage in Yemen." Genetics 150, no. 2 (October 1, 1998): 835–61. http://dx.doi.org/10.1093/genetics/150.2.835.

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Abstract The mitochondrial DNA (mtDNA) control region and flanking tRNAs were sequenced from 76 mice collected at 60 localities extending from Egypt through Turkey, Yemen, Iran, Afghanistan, Pakistan, and Nepal to eastern Asia. Segments of the Y chromosome and of a processed p53 pseudogene (ψp53) were amplified from many of these mice and from others collected elsewhere in Eurasia and North Africa. The 251 mtDNA types, including 54 new ones reported here, now identified from commensal house mice (Mus musculus group) by sequencing this segment can be organized into four major lineages—domesticus, musculus, castaneus, and a new lineage found in Yemen. Evolutionary tree analysis suggested the domesticus mtDNAs as the sister group to the other three commensal mtDNA lineages and the Yemeni mtDNAs as the next oldest lineage. Using this tree and the phylogeographic approach, we derived a new model for the origin and radiation of commensal house mice whose main features are an origin in west-central Asia (within the present-day range of M. domesticus) and the sequential spreading of mice first to the southern Arabian Peninsula, thence eastward and northward into south-central Asia, and later from south-central Asia to north-central Asia (and thence into most of northern Eurasia) and to southeastern Asia. Y chromosomes with and without an 18-bp deletion in the Zfy-2 gene were detected among mice from Iran and Afghanistan, while only undeleted Ys were found in Turkey, Yemen, Pakistan, and Nepal. Polymorphism for the presence of a ψp53 was observed in Georgia, Iran, Turkmenistan, Afghanistan, and Pakistan. Sequencing of a 128-bp ψp53 segment from 79 commensal mice revealed 12 variable sites and implicated ≥14 alleles. The allele that appeared to be phylogenetically ancestral was widespread, and the greatest diversity was observed in Turkey, Afghanistan, Pakistan, and Nepal. Two mice provided evidence for a second ψp53 locus in some commensal populations.

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35

Butterfield, Russell J., Randall J. Roper, Dominic M. Rhein, Roger W. Melvold, Lia Haynes, Runlin Z. Ma, R. W. Doerge, and Cory Teuscher. "Sex-Specific Quantitative Trait Loci Govern Susceptibility to Theiler’s Murine Encephalomyelitis Virus-Induced Demyelination." Genetics 163, no. 3 (March 1, 2003): 1041–46. http://dx.doi.org/10.1093/genetics/163.3.1041.

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Abstract Susceptibility to Theiler’s murine encephalomyelitis virus-induced demyelination (TMEVD), a mouse model for multiple sclerosis (MS), is genetically controlled. Through a mouse-human comparative mapping approach, identification of candidate susceptibility loci for MS based on the location of TMEVD susceptibility loci may be possible. Composite interval mapping (CIM) identified quantitative trait loci (QTL) controlling TMEVD severity in male and female backcross populations derived from susceptible DBA/2J and resistant BALBc/ByJ mice. We report QTL on chromosomes 1, 5, 15, and 16 affecting male mice. In addition, we identified two QTL in female mice located on chromosome 1. Our results support the existence of three linked sex-specific QTL on chromosome 1 with opposing effects on the severity of the clinical signs of TMEV-induced disease in male and female mice.

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Figueroa, Felipe, Masanori Kasahara, Herbert Tichy, Esther Neufeld, Uzi Ritte, and Jan Klein. "Polymorphism of Unique Noncoding DNA Sequences in Wild and Laboratory Mice." Genetics 117, no. 1 (September 1, 1987): 101–8. http://dx.doi.org/10.1093/genetics/117.1.101.

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ABSTRACT Two DNA probes, D17Tul and D17Tu2, were isolated from a genomic DNA library containing only two mouse chromosomes, one of which is chromosome 17, carrying the major histocompatibility complex (H-2), as well as the t complex genes. The D17Tul probe was mapped to the centromeric region of chromosome 17 and the D17Tu2 probe to the S region of the H-2 complex. Neither of the two probes appeared to detect any genes, but both contained unique, nonrepetitive sequences. Typing of DNA obtained from a large panel of mice revealed the presence of four D17Tul patterns in inbred mouse strains, one very common, one less common, and two present in one strain each. The two common patterns could not be detected in appreciable frequencies in the European wild mice tested (one of the two patterns was, however, found in Australian wild mice). Conversely, the patterns found frequently in European wild mice are absent in the laboratory mice. We therefore conclude that wild mice from the sampled regions of Europe could not have provided the ancestral stocks from which inbred strains were derived. Only one D17Tul pattern was found in all the populations of Mus musculus tested, while eight patterns were found in Mus domesticus, with virtually all the populations being polymorphic. We suggest that this difference reflects different modes in which the two species colonized Europe. The distribution of the D17Tu2 patterns in inbred strains correlates with the distribution of H-2 haplotypes.

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Alagramam, K. N., H. Y. Kwon, N. L. A. Cacheiro, L. Stubbs, C. G. Wright, L. C. Erway, and R. P. Woychik. "A New Mouse Insertional Mutation That Causes Sensorineural Deafness and Vestibular Defects." Genetics 152, no. 4 (August 1, 1999): 1691–99. http://dx.doi.org/10.1093/genetics/152.4.1691.

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Abstract This article describes a new recessive insertional mutation in the transgenic line TgN2742Rpw that causes deafness and circling behavior in mice. Histologic analysis revealed virtually complete loss of the cochlear neuroepithelium (the organ of Corti) in adult mutant mice. In association with the neuroepithelial changes, there is a dramatic reduction of the cochlear nerve supply. Adult mutants also show morphological defects of the vestibular apparatus, including degeneration of the saccular neuroepithelium and occasional malformation of utricular otoconia. Audiometric evaluations demonstrated that the mice displaying the circling phenotype are completely deaf. Molecular analysis of this mutant line revealed that the transgenic insertion occurred without creating a large deletion of the host DNA sequences. The mutant locus was mapped to a region on mouse chromosome 10, where other spontaneous, recessive mutations causing deafness in mice have been mapped.

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Wang, Lan, Charles E. Ogburn, Carol B. Ware, Warren C. Ladiges, Hagop Youssoufian, George M. Martin, and Junko Oshima. "Cellular Werner Phenotypes in Mice Expressing a Putative Dominant-Negative Human WRN Gene." Genetics 154, no. 1 (January 1, 2000): 357–62. http://dx.doi.org/10.1093/genetics/154.1.357.

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Abstract Mutations at the Werner helicase locus (WRN) are responsible for the Werner syndrome (WS). WS patients prematurely develop an aged appearance and various age-related disorders. We have generated transgenic mice expressing human WRN with a putative dominant-negative mutation (K577M-WRN). Primary tail fibroblast cultures from K577M-WRN mice showed three characteristics of WS cells: hypersensitivity to 4-nitroquinoline-1-oxide (4NQO), reduced replicative potential, and reduced expression of the endogenous WRN protein. These data suggest that K577M-WRN mice may provide a novel mouse model for the WS.

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Atchley, William R., and Jun Zhu. "Developmental Quantitative Genetics, Conditional Epigenetic Variability and Growth in Mice." Genetics 147, no. 2 (October 1, 1997): 765–76. http://dx.doi.org/10.1093/genetics/147.2.765.

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Ontogenetic variation in the causal components of phenotypic variability and covariability is described for body weight and tail length in mice derived from a full 7 × 7 diallel cross. Age-related changes in additive, dominance, sex-linked and maternal variance and covariance between 14 and 70 days of age are described. Age-specific variance components at time t are conditioned on the causal genetic effects at time (t – 1). This procedure demonstrates the generation of significant episodes of new genetic variation arising at specific intervals during ontogeny. These episodes of new genetic variation are placed in the context of epigenetic models in developmental quantitative genetics. These results are also concordant on recent findings on age-specific gene expression in mouse growth as shown by QTL analyses.

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Atchley, William R., Shizhong Xu, and David E. Cowley. "Altering Developmental Trajectories in Mice by Restricted Index Selection." Genetics 146, no. 2 (June 1, 1997): 629–40. http://dx.doi.org/10.1093/genetics/146.2.629.

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A restricted index selection experiment on mice was carried out for 14 generations on rate of early postnatal development (growth rate from birth to 10 days of age) vs. rate of development much later in ontogeny (growth rate from 28 to 56 days of age). Early rate of development (E) approximates hyperplasia (changes in cell number) and later rate (L) reflects hypertropy (changes in cell size). The selection criteria were as follows: E+L0 was selected to increase early body weight gain while holding late body weight gain constant; E–L0 was selected to decrease early body gain while holding late gain constant; E0L+ was selected to increase late gain holding early gain constant; and E0L– was selected to decrease late gain holding early gain constant. After 14 generations of selection, significant divergence among lines has occurred and the changes in the growth trajectories are very close to expectation. The genetic and developmental bases of complex traits are discussed as well as the concept of developmental homoplasy.

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41

Dear, K. B., M. Salazar, A. L. Watson, R. S. Gelman, R. Bronson, and E. J. Yunis. "Traits that influence longevity in mice: a second look." Genetics 132, no. 1 (September 1, 1992): 229–39. http://dx.doi.org/10.1093/genetics/132.1.229.

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Abstract Analysis of genetic interactions in the F2 of an intercross of (C57BL/6 x DBA/2) F1J revealed influences of genetic factors on life span. Females lived longer than males. Dilute brown females died sooner than females of other colors. H-2b/H-2b males died sooner than H-2b/H-2d or H-2d/H-2d males, except that among dilute brown males those of typeH-2b/H-2d died sooner. Cluster analysis suggested that male and female genotypes each fall into two groups, with female dilute brown mice having shorter lives than other females, and male H-2b/H-2b mice except dilute brown and dilute brown H-2b/H-2d mice having shorter lives than other males. The association of heterozygosity with life span was clearer in females than in males, yet the longest-lived female genotype was homozygous H-2d/H-2d, of dominant Black phenotype at the Brown locus of chromosome 4, and homozygous dd at the Dilute locus of chromosome 9. The shortest-lived females were dilute brown H-2b/H-2b. The longest-lived and shortest-lived male genotypes were dilute brown H-2d/H-2d and dilute brown H-2b/H-2d, respectively. Although histological findings at postmortem differed between the sexes, there was no association of particular disorders with other genetic markers. The importance of H-2 in males was confirmed, but the allelic effects were perturbed, possibly by the absence of Sendai infection in this experiment. Overall our studies suggest that genetic influences on life span involve interactions between loci, and allelic interactions may change with viral infections or other environmental factors.

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42

Bedell, Mary A., Linda S. Cleveland, T. Norene O'Sullivan, Neal G. Copeland, and Nancy A. Jenkins. "Deletion and Interallelic Complementation Analysis of Steel Mutant Mice." Genetics 142, no. 3 (March 1, 1996): 935–44. http://dx.doi.org/10.1093/genetics/142.3.935.

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Abstract Mutations at the Steel (Sl) locus produce pleiotropic effects on viability as well as hematopoiesis, pigmentation and fertility. Several homozygous viable Sl alleles have previously been shown to contain either structural alterations in mast cell growth factor (Mgf) or regulatory mutations that affect expression of the Mgf gene. More severe Sl alleles cause lethality to homozygous embryos and all lethal Sl alleles examined to date contain deletions that remove the entire Mgf coding region. As the timing of the lethality varies from early to late in gestation, it is possible that some deletions may affect other closely linked genes in addition to Mgf We have analyzed the extent of deleted sequences in seven homozygous lethal Sl alleles. The results of this analysis suggest that late gestation lethality represents the Sl null phenotype and that pen-implantation lethality results from the deletion of at least one essential gene that maps proximal to Sl. We have also examined gene dosage effects of Sl by comparing the phenotypes of mice homozygous and hemizygous for each of four viable Sl alleles. Lastly, we show that certain combinations of the viable Sl alleles exhibit interallelic complementation. Possible mechanisms by which such complementation could occur are discussed.

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43

Wang, Richard J., Michael A. White, and Bret A. Payseur. "The Pace of Hybrid Incompatibility Evolution in House Mice." Genetics 201, no. 1 (July 20, 2015): 229–42. http://dx.doi.org/10.1534/genetics.115.179499.

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44

Valdar, William, Leah C. Solberg, Dominique Gauguier, William O. Cookson, J. Nicholas P. Rawlins, Richard Mott, and Jonathan Flint. "Genetic and Environmental Effects on Complex Traits in Mice." Genetics 174, no. 2 (August 3, 2006): 959–84. http://dx.doi.org/10.1534/genetics.106.060004.

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45

Osato, Naoki, Yoshiyuki Suzuki, Kazuho Ikeo, and Takashi Gojobori. "Transcriptional Interferences incisNatural Antisense Transcripts of Humans and Mice." Genetics 176, no. 2 (April 3, 2007): 1299–306. http://dx.doi.org/10.1534/genetics.106.069484.

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46

Bao-Cutrona, M., and P. Moral. "Unexpected Expression Pattern of Tetracycline-Regulated Transgenes in Mice." Genetics 181, no. 4 (February 9, 2009): 1687–91. http://dx.doi.org/10.1534/genetics.108.097600.

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47

Dumont, Beth L., Karl W. Broman, and Bret A. Payseur. "Variation in Genomic Recombination Rates Among Heterogeneous Stock Mice." Genetics 182, no. 4 (June 17, 2009): 1345–49. http://dx.doi.org/10.1534/genetics.109.105114.

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48

Carbery, Iara D., Diana Ji, Anne Harrington, Victoria Brown, Edward J. Weinstein, Lucy Liaw, and Xiaoxia Cui. "Targeted Genome Modification in Mice Using Zinc-Finger Nucleases." Genetics 186, no. 2 (July 13, 2010): 451–59. http://dx.doi.org/10.1534/genetics.110.117002.

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49

Casellas, Joaquim, Rodrigo J. Gularte, Charles R. Farber, Luis Varona, Margarete Mehrabian, Eric E. Schadt, Aldon J. Lusis, Alan D. Attie, Brian S. Yandell, and Juan F. Medrano. "Genome Scans for Transmission Ratio Distortion Regions in Mice." Genetics 191, no. 1 (February 23, 2012): 247–59. http://dx.doi.org/10.1534/genetics.111.135988.

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50

Nadeau, Joseph H. "A GLYOXALASE-1 VARIANT ASSOCIATED WITH THE t-COMPLEX IN HOUSE MICE." Genetics 113, no. 1 (May 1, 1986): 91–99. http://dx.doi.org/10.1093/genetics/113.1.91.

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ABSTRACT A quantitative variant of glyoxalase-1 associated with the t-complex in house mice is described. GLO-1C in red cell lysates from mice heterozygous for complementing t-haplotypes and from mice homozygous for the tw 8-haplotype had less than one-third the GLO-1 activity of NZB/BINJ, the inbred strain with the lowest activity previously reported. GLO-1C appeared to be determined by the structural locus Glo-1 and, together with two partial t 6-haplotypes, was used to map Glo-1 to the telomeric portion of the t 6-haplotype. Glo-1c was associated with all t-haplotypes tested and has not been found in mice that lack a t-complex. Thus, this variant of Glo-1c provides both a further example of gametic disequilibrium between the t-complex and linked loci and a readily identifiable marker for the t-complex.

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