scholarly journals Novel Genetic Loci Control Calcium Absorption and Femur Bone Mass as Well as Their Response to Low Calcium Intake in Male BXD Recombinant Inbred Mice

2016 ◽  
Vol 31 (5) ◽  
pp. 994-1002 ◽  
Author(s):  
Perla C Reyes Fernandez ◽  
Rebecca A Replogle ◽  
Libo Wang ◽  
Min Zhang ◽  
James C Fleet
Keyword(s):  
Bone Mass ◽  
Calcium Intake ◽  
Recombinant Inbred ◽  
Calcium Absorption ◽  
Inbred Mice ◽  
Genetic Loci ◽  
Femur Bone ◽  
Recombinant Inbred Mice ◽  
Low Calcium

scholarly journals BXD Recombinant Inbred Mice as a Model to Study Neurotoxicity

Biomolecules ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 1762
Author(s):  
Airton C. Martins ◽  
Caridad López-Granero ◽  
Beatriz Ferrer ◽  
Alexey A. Tinkov ◽  
Anatoly V. Skalny ◽  
...  
Keyword(s):  
Recombinant Inbred ◽  
Inbred Mice ◽  
Reference Population ◽  
Recombinant Inbred Mice ◽  
Complex Phenotypes ◽  
Pesticide Exposures ◽  
Underlying Mechanisms ◽  
Genomic Locations ◽  
Segregating Population ◽  
Ri Lines

BXD recombinant inbred (RI) lines represent a genetic reference population derived from a cross between C57BL/6J mice (B6) and DBA/2J mice (D2), which through meiotic recombination events possesses recombinant chromosomes containing B6 or D2 haplotype segments. The quantitative trait loci (QTLs) are the locations of segregating genetic polymorphisms and are fundamental to understanding genetic diversity in human disease susceptibility and severity. QTL mapping represents the typical approach for identifying naturally occurring polymorphisms that influence complex phenotypes. In this process, genotypic values at markers of known genomic locations are associated with phenotypic values measured in a segregating population. Indeed, BXD RI strains provide a powerful tool to study neurotoxicity induced by different substances. In this review, we describe the use of BXD RI lines to understand the underlying mechanisms of neurotoxicity in response to ethanol and cocaine, as well as metals and pesticide exposures.

Genetic Regulation ofMycobacterium paratuberculosisInfection in Recombinant Inbred Mice

1990 ◽  
Vol 27 (5) ◽  
pp. 362-364 ◽  
Author(s):  
P. F. Frelier ◽  
J. W. Templeton ◽  
M. Estes ◽  
H. W. Whitford ◽  
R. D. Kienle
Keyword(s):  
Recombinant Inbred ◽  
Inbred Mice ◽  
Genetic Regulation ◽  
Recombinant Inbred Mice

scholarly journals Cmv-1, a genetic locus that controls murine cytomegalovirus replication in the spleen.

1990 ◽  
Vol 171 (5) ◽  
pp. 1469-1483 ◽  
Author(s):  
A A Scalzo ◽  
N A Fitzgerald ◽  
A Simmons ◽  
A B La Vista ◽  
G R Shellam
Keyword(s):  
Distribution Pattern ◽  
Recombinant Inbred ◽  
Strain Distribution ◽  
Inbred Mice ◽  
Genetic Locus ◽  
Murine Cytomegalovirus ◽  
Mcmv Infection ◽  
Strain Distribution Pattern ◽  
Recombinant Inbred Mice ◽  
Hsv 1

The genetic basis of the control of acute splenic MCMV infection was studied after intraperitoneal inoculation of the virus. Classical Mendelian analyses using C57BL/6 (resistant) and BALB/c (susceptible) parental strains disclosed an autosomal dominant non-H-2 gene that regulates splenic virus replication. The probable location of this gene, to which we have assigned the symbol Cmv-1, is on chromosome 6 as defined by the strain distribution pattern of splenic MCMV replication in CXB recombinant inbred mice. Although there is a similar hierarchy of resistance to MCMV and HSV-1 with respect to the C57BL and BALB genetic backgrounds, the strain distribution pattern of HSV-1 replication in recombinant inbred mice suggests that Cmv-1 is not involved in restricting the spread of this virus. This is the first clear identification of a non-H-2 gene regulating the magnitude of MCMV infection. Elucidation of the function of this gene may be a fundamental step towards understanding the control of systemic CMV infection.

scholarly journals Age-related thymic involution in C57BL/6J × DBA/2J recombinant-inbred mice maps to mouse chromosomes 9 and 10

2003 ◽  
Vol 4 (6) ◽  
pp. 402-410 ◽  
Author(s):  
H-C Hsu ◽  
H-G Zhang ◽  
L Li ◽  
N Yi ◽  
P-A Yang ◽  
...  
Keyword(s):  
Recombinant Inbred ◽  
Inbred Mice ◽  
Thymic Involution ◽  
Recombinant Inbred Mice ◽  
Age Related

scholarly journals Spontaneous Mutations in Recombinant Inbred Mice: Mutant Toll-like Receptor 4 (Tlr4) in BXD29 Mice

Genetics ◽  
2005 ◽  
Vol 172 (3) ◽  
pp. 1751-1755 ◽  
Author(s):  
Donald N. Cook ◽  
Gregory S. Whitehead ◽  
Lauranell H. Burch ◽  
Katherine G. Berman ◽  
Zareen Kapadia ◽  
...  
Keyword(s):  
Recombinant Inbred ◽  
Inbred Mice ◽  
Spontaneous Mutations ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Recombinant Inbred Mice

Erratum to “Genetic influences on hippocampal structure and function in recombinant inbred mice” [Behav. Brain Res. 196 (2009) 78–83]

2009 ◽  
Vol 199 (2) ◽  
pp. 364
Author(s):  
Maureen V. Martin ◽  
James D. Churchill ◽  
Hongxin Dong ◽  
David F. Wozniak ◽  
James M. Cheverud ◽  
...  
Keyword(s):  
Recombinant Inbred ◽  
Inbred Mice ◽  
Structure And Function ◽  
Genetic Influences ◽  
Recombinant Inbred Mice ◽  
And Function ◽  
Hippocampal Structure

Mapping of Genes That Control the Antibody Response to Human FVIII in Mice.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 1888-1888
Author(s):  
Jay Nelson Lozier ◽  
Pei Zhang
Keyword(s):  
Antibody Response ◽  
Mouse Chromosome ◽  
Recombinant Inbred ◽  
Inbred Mice ◽  
Antibody Responses ◽  
Polymorphic Markers ◽  
Suggestive Linkage ◽  
Lod Score ◽  
Male And Female ◽  
Recombinant Inbred Mice

Abstract In our previous studies of genetic factors that influence the immune response (particularly inhibitor antibodies) to therapeutic coagulation factors we have shown that H2 and cytokine genes control the antibody response to human FIX protein in mice (Lozier et al., Blood105:1029–1035, 2005). We have extended our investigation to the murine resonse to human FVIII. Based on the observation that FVIII K/O mice in Balb/cByJ and C57BL/6ByJ backgrounds have significantly different antibody responses to human FVIII after gene transfer (Brown et al., J Thromb Haemost2:111–8, 2004) we studied the antibody response to human FVIII in these mice and 13 CXB recombinant inbred mouse lines derived from these parental strains. Balb/cByJ mice were significantly higher responders to human FVIII than C57BL/6ByJ mice after a single injection with an adenovirus vector (AVPGKf8mg) expressing human FVIII (P < 0.001) or serial intravenous injections of human FVIII protein sans adjuvant (P < 0.01). For both strains the difference between male and female antibody responses following adenovirus or FVIII protein injections were not significantly different. Phage display mapping with 7-mer looped and 12-mer linear libraries showed reactivity against epitopes in the A1, A2, B, and C1 domains of human FVIII as well as the acidic region between the A1/A2 domains, after administration of FVIII protein. Analysis of antibody titers to human FVIII in male CXB recombinant inbred mice after weight-adjusted doses of AVPGKF8mg vector revealed suggestive linkage-relatedness scores for a series of polymorphic markers on mouse chromosome 8 that are 40–45 centimorgans from the centromere. These include D8mit 240 (LOD score 3.1), D8mit45 (LOD score 3.1), and D8mit84 (LOD score 3.0). Each marker had an equal additive effect to the antibody response. In female CXB recombinant inbred mice different markers were associated with the antibody response to FVIII than in males. For female CXB recombinant inbred mice there were suggestive linkage relatedness scores for polymorphic markers on mouse chromosome 17 (D17mit16, LOD score 3.0) and mouse chromosome 5 (D5mit31, LOD score 2.4). Both markers had equal additive effects on the antibody response to human FVIII. D17mit16 is adjacent to the mouse H2 gene complex, an obvious candidate for genetic control of the immune response. D5mit31 is a polymorphic marker associated with the zinc alpha-2-glycoprotein I (AZGP) gene on mouse chromosome 5. AZGP is a 307 amino acid plasma glycoprotein whose physiologic function involves regulation of lipolysis. It has homology to class I protein in its amino terminus and to the immunoglobulin constant domain at its carboxy terminus. AZGP binds lipids and zinc, which raises the possibility that it may relate to FVIII protein by mutual interaction with lipids and/or transition metals (e.g., copper/zinc). Our FVIII antibody linkage results differs from our previous work with FIX in that the linkage scores are not as high for the anti-FVIII response as for the anti-FIX response. Further, in this study there are different polymorphic markers associated with the antibody response in male and female mice. We continue to investigate genes in mice that control the antibody response to factors VIII and IX in order to identify and predict candidate genes that should be investigated in higher animal models of hemophilia (e.g., hemophilia A and B dogs) as well as in humans with hemophilia.

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