scholarly journals Human histone 3 F2 detects RFLPs in inbred mice, cosegregates with H4F2 and does not map to possible syntenic groups on mouse distal chromosome 1 and distal chromosome 3

1987 ◽  
Vol 15 (14) ◽  
pp. 5900-5900 ◽  
Author(s):  
M.F. Seldin ◽  
A.D. Steinberg
Keyword(s):  
Inbred Mice ◽  
Chromosome 1 ◽  
Chromosome 3 ◽  
Histone 3 ◽  
Distal Chromosome

Low-penetrance genetic susceptibility and resistance loci implicated in the relative risk for radiation-induced acute myeloid leukemia in mice

Blood ◽  
2003 ◽  
Vol 101 (6) ◽  
pp. 2349-2354 ◽  
Author(s):  
Emma Boulton ◽  
Clare Cole ◽  
Abigail Knight ◽  
Helen Cleary ◽  
Roger Snowden ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Relative Risk ◽  
Myeloid Leukemia ◽  
Inbred Mice ◽  
Chromosome 1 ◽  
Chromosome 6 ◽  
A Genome ◽  
Distal Chromosome ◽  
Radiation Induced ◽  
Acute Myeloid

Inbred CBA/H mice are susceptible to radiation-induced acute myeloid leukemia (r-AML), and C57BL/6 mice are resistant. A genome-wide screen for linkage between genotype and phenotype (r-AML) of 67 affected (CBA/H × C57BL/6)F1 × CBA/H backcross mice has revealed at least 2 suggestive loci that contribute to the overall lifetime risk for r-AML. Neither is necessary or sufficient for r-AML, but relative risk is the net effect of susceptibility (distal chromosome 1) and resistance (chromosome 6) loci. An excess of chromosome 6 aberrations in mouse r-AML and bone marrow cells up to 6 months after irradiation in vivo suggests the locus confers a proliferative advantage during the leukemogenic process. The stem cell frequency regulator 1 (Scfr1) locus maps to distal chromosome 1 and determines the frequency of hemopoietic stem cells (HSCs) in inbred mice, suggesting that target size may be one factor in determining the relative susceptibility of inbred mice to r-AML.

scholarly journals Terc Gene Cluster Variants Predict Liver Telomere Length in Mice

Cells ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 2623
Author(s):  
Dana Zeid ◽  
Sean Mooney-Leber ◽  
Laurel R. Seemiller ◽  
Lisa R. Goldberg ◽  
Thomas J. Gould
Keyword(s):  
Linkage Disequilibrium ◽  
Telomere Length ◽  
Gene Cluster ◽  
Inbred Mice ◽  
Inbred Mouse ◽  
Mouse Strains ◽  
Chromosome 3 ◽  
Human Populations ◽  
Nucleotide Polymorphisms ◽  
Initial Finding

Variants in a gene cluster upstream-adjacent to TERC on human chromosome 3, which includes genes APRM, LRRC31, LRRC34 and MYNN, have been associated with telomere length in several human populations. Currently, the mechanism by which variants in the TERC gene cluster influence telomere length in humans is unknown. Given the proximity between the TERC gene cluster and TERC (~0.05 Mb) in humans, it is speculated that cluster variants are in linkage disequilibrium with a TERC causal variant. In mice, the Terc gene/Terc gene cluster are also located on chromosome 3; however, the Terc gene cluster is located distantly downstream of Terc (~60 Mb). Here, we initially aim to investigate the interactions between genotype and nicotine exposure on absolute liver telomere length (aTL) in a panel of eight inbred mouse strains. Although we found no significant impact of nicotine on liver aTL, this first experiment identified candidate single nucleotide polymorphisms (SNPs) in the murine Terc gene cluster (within genes Lrrc31, Lrriq4 and Mynn) co-varying with aTL in our panel. In a second experiment, we tested the association of these Terc gene cluster variants with liver aTL in an independent panel of eight inbred mice selected based on candidate SNP genotype. This supported our initial finding that Terc gene cluster polymorphisms impact aTL in mice, consistent with data in human populations. This provides support for mice as a model for telomere dynamics, especially for studying mechanisms underlying the association between Terc cluster variants and telomere length. Finally, these data suggest that mechanisms independent of linkage disequilibrium between the Terc/TERC gene cluster and the Terc/TERC gene mediate the cluster’s regulation of telomere length.

Mapping colitis susceptibility in mouse models: distal chromosome 3 contains major loci related to Cdcs1

2013 ◽  
Vol 45 (20) ◽  
pp. 925-930 ◽  
Author(s):  
Manuela Buettner ◽  
André Bleich
Keyword(s):  
Mouse Models ◽  
Genetic Mutation ◽  
Chromosome 3 ◽  
Environmental Interactions ◽  
Causative Factors ◽  
Distal Chromosome ◽  
Pathogen Control ◽  
Inflammatory Bowel ◽  
Trait Locus ◽  
Relevant Factors

Inflammatory bowel disease (IBD) summarizes a group of chronic intestinal disorders with Crohn's disease and ulcerative colitis being most prominent. Though much effort is put into identification of causative factors, its etiology is still not understood. Risk factors for disease development include genetic predisposition and environmental triggers. Crucial for identification and analysis of relevant factors are mouse models. Experimental IBD in mice occurs spontaneously or is induced by chemicals, cell transfer, pathogens, or genetic mutation. These models were utilized for analyzing genetic contribution to disease and genotype-environmental interactions. In these studies, a variety of modifier loci were identified, thereby demonstrating the complexity of disease. A major contribution of distal chromosome 3 was independently replicated in several studies. The first colitogenic QTL in this region was detected using the IL-10-deficient mouse model and called cytokine deficiency-induced colitis susceptibility ( Cdcs) 1. This quantitative trait locus contains at least three subintervals with independent genetic factors. This locus or defined subintervals were replicated in at least seven studies, using models based on dysregulation of innate or adaptive immunity or pathogen control. In this review we illustrate the various models used for genetic mapping of susceptibility to experimental IBD and display Cdcs1-related loci as well as the mechanism of their contribution identified so far.

scholarly journals Severity of Tuberculosis in Mice is Linked to Distal Chromosome 3 and Proximal Chromosome 9

1999 ◽  
Vol 180 (1) ◽  
pp. 150-155 ◽  
Author(s):  
Catharina Lavebratt ◽  
Alexander S. Apt ◽  
Boris V. Nikonenko ◽  
Martin Schalling ◽  
Erwin Schurr
Keyword(s):  
Chromosome 9 ◽  
Chromosome 3 ◽  
Distal Chromosome

scholarly journals Characterization of Nob3, a major quantitative trait locus for obesity and hyperglycemia on mouse chromosome 1

2009 ◽  
Vol 38 (2) ◽  
pp. 226-232 ◽  
Author(s):  
Heike Vogel ◽  
Matthias Nestler ◽  
Franz Rüschendorf ◽  
Marcel-Dominique Block ◽  
Sina Tischer ◽  
...  
Keyword(s):  
Quantitative Trait Locus ◽  
Body Weight ◽  
Body Fat ◽  
Quantitative Trait ◽  
Plasma Cholesterol ◽  
Chromosome 1 ◽  
Nzo Mice ◽  
Distal Chromosome ◽  
Trait Locus ◽  
Haplotype Mapping

New Zealand obese (NZO) mice present a metabolic syndrome of obesity, insulin resistance, and diabetes. To identify chromosomal segments associated with these traits, we intercrossed NZO mice with the lean and diabetes-resistant C57BL/6J (B6) strain. Obesity and hyperglycemia in the (NZO×B6)F2 intercross population were predominantly due to a broad quantitative trait locus (QTL) on chromosome 1 ( Nob3; logarithm of the odds score 16.1, 16.0, 4.0 for body weight, body fat, and blood glucose, respectively), producing a difference between genotypes of 12.7 or 5.2 g of body weight and 12.0 or 4.0 g of body fat in females or males, respectively. In addition, significant QTL on chromosomes 3 and 13 and suggestive QTL on chromosomes 4, 6, 9, 12, 14, and 19 contributed to the obese phenotype. Distal chromosome 5 was significantly linked with plasma cholesterol (LOD score 10.7). Introgression of two segments of Nob3 into B6 confirmed the adipogenic effect of the QTL and suggested the presence of at least one causal gene. Haplotype mapping reduced the critical region of the distal part of the QTL to 31 Mbp containing the potential candidates Nr1i3, Apoa2, Atp1a2, Prox1, and Hsd11b1. We conclude that obesity and hyperglycemia of NZO is to a large part caused by variant genes located in Nob3 on chromosome 1. Since these exert robust effects on a B6 background, the QTL Nob3 is a prime target for identification of a novel diabesity gene.

Localization of the mouse gene encoding tyrosine kinase receptor type 10 on distal Chromosome 1

1997 ◽  
Vol 8 (12) ◽  
pp. 941-942 ◽  
Author(s):  
Jennifer N. Murdoch ◽  
Jane Eddleston ◽  
Philip Stanier ◽  
Andrew J. Copp
Keyword(s):  
Tyrosine Kinase ◽  
Mouse Gene ◽  
Receptor Type ◽  
Chromosome 1 ◽  
Tyrosine Kinase Receptor ◽  
Gene Encoding ◽  
Distal Chromosome

Specific end-to-end attachment of chromosomes in Ornithogalum virens

1979 ◽  
Vol 38 (1) ◽  
pp. 357-367
Author(s):  
T. Ashley
Keyword(s):  
Chromosome 1 ◽  
Chromosome 3 ◽  
Chromosome 2 ◽  
Root Tips ◽  
End To End ◽  
Specific Association ◽  
High Degree ◽  
Ornithogalum Virens ◽  
Homologous Alignment ◽  
Generative Nuclei

C-banding of nonhomologous chromosomes in haploid generative nuclei of Ornithogalum virens (n = 3) reveals a high degree of specificity with respect to end-to-end connexions. The centromeric end of chromosome 2 preferentially associates with the centromeric end of chromosome 3 and the telomeric end of chromosome 3 associates preferentially with the telomeric end of chromosome 1. This same association of nonhomologous chromosomes persists in prophase nuclei of diploid root tips. In addition, the telomeric ends of the 2 chromosome 2s are connected to one another as are the centromeric ends of the chromosome 1s. This results in a ring of chromosomes in which homologues lie opposite one another. Centromeric ends lie on one side of the nucleus and telomeric ends on the other. It is proposed that this specific association of chromosome ends reflects an order which was probably established at the preceding anaphase or telophase and which persists throughout interphase. The suggestion is made that the proximity of homologous ends and consequently homologous alignment may facilitate initiation of pairing at meiosis.

Discordant Rates of Chromosome Evolution in the Drosophila virilis Species Group

Genetics ◽  
1997 ◽  
Vol 147 (1) ◽  
pp. 223-230 ◽  
Author(s):  
Jorge Vieira ◽  
Cristina P Vieira ◽  
Daniel L Hartl ◽  
Elena R Lozovskaya
Keyword(s):  
Polytene Chromosome ◽  
Genomic Dna ◽  
Chromosome Evolution ◽  
Species Group ◽  
Drosophila Virilis ◽  
Chromosome 1 ◽  
Chromosome 3 ◽  
Bacteriophage P1 ◽  
Minimum Number ◽  
Chromosome Maps

Abstract In Drosophila, the availability of polytene chromosome maps and of sets of probes covering most regions of the chromosomes allows a direct comparison of the organization of the genome in different species. In this work, we report the localization, in Drosophila virilis, D. montana, and D. novamexicana, of >100 bacteriophage P1 clones containing ~65 kilobase inserts of genomic DNA from D. virilis. Each clone hybridizes with a single euchromatic site in either chromosome 1 or chromosome 3 in D. virilis. From these data, it is possible to estimate the minimum number of inversions required to transform the map positions of the probes in one species into the map positions of the same probes in a related species. The data indicate that, in the D. virilis species group, the X chromosome has up to four times the number of inversions as are observed in chromosome 3. The first photographic polytene chromosome maps for D. montana and D. novamexicana are also presented.

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