High-resolution genetic map of mouse Chromosome 1 between D1MU227 and D1Mit15 by use of an intercross of C57BL/6J × C3HeB/FeJ vl/vl

1996 ◽  
Vol 7 (10) ◽  
pp. 770-770 ◽  
Author(s):  
J. -L. Mu ◽  
T. Gilley ◽  
R. Turner ◽  
B. Paigen
Genomics ◽  
2001 ◽  
Vol 78 (3) ◽  
pp. 197-205 ◽  
Author(s):  
Christopher Hayes ◽  
Andreas Rump ◽  
Matthew R. Cadman ◽  
Mark Harrison ◽  
Edward P. Evans ◽  
...  

Genomics ◽  
1990 ◽  
Vol 7 (1) ◽  
pp. 57-64 ◽  
Author(s):  
B. Mock ◽  
M. Krall ◽  
J. Blackwell ◽  
A. O'Brien ◽  
E. Schurr ◽  
...  

1990 ◽  
Vol 172 (1) ◽  
pp. 263-272 ◽  
Author(s):  
M L Watson ◽  
S F Kingsmore ◽  
G I Johnston ◽  
M H Siegelman ◽  
M M Le Beau ◽  
...  

A structurally and functionally related group of genes, lymph node homing receptor (LHR), granule membrane protein 140 (GMP-140), and endothelial leukocyte adhesion molecule 1 (ELAM-1) are shown to constitute a gene cluster on mouse and human chromosome 1. In situ hybridization mapped GMP-140 to human chromosome 1 bands 21-24 consistent with chromosomal localization of LHR. Gene linkage analysis in the mouse indicated that these genes and serum coagulation factor V (FV) all map to a region of distal mouse chromosome 1 that is syntenic with human chromosome 1, with no crossovers identified between these four genes in 428 meiotic events. Moreover, long range restriction site mapping demonstrated that these genes map to within 300 kb in both the human and mouse genomes. These data suggest that LHR, ELAM-1, and GMP-140 comprise an adhesion protein family, the selectins, that arose by multiple gene duplication events before divergence of mouse and human. Furthermore, the location of these genes on mouse and human chromosome 1 is consistent with a close evolutionary relationship to the complement receptor-related genes, which also are positioned on the same chromosomes in both species and with which these genes share a region of sequence homology. These data characterize the organization of a genomic region that may be critical for intercellular communication within the immune system.


1988 ◽  
Vol 47 (1-2) ◽  
pp. 11-15 ◽  
Author(s):  
B.A. Mock ◽  
D. Givol ◽  
L.A. Dhoostelaere ◽  
K. Huppi ◽  
M.F. Seldin ◽  
...  

2012 ◽  
Vol 113 (1) ◽  
pp. 167-174 ◽  
Author(s):  
C. Barton Gillombardo ◽  
Motoo Yamauchi ◽  
Mark D. Adams ◽  
Jesse Dostal ◽  
Sam Chai ◽  
...  

Although central to the susceptibility of adult diseases characterized by abnormal rhythmogenesis, characterizing the genes involved is a challenge. We took advantage of the C57BL/6J (B6) trait of hypoxia-induced periodic breathing and its absence in the C57BL/6J-Chr 1A/J/NaJ chromosome substitution strain to test the feasibility of gene discovery for this abnormality. Beginning with a genetic and phenotypic analysis of an intercross study between these strains, we discovered three quantitative trait loci (QTLs) on mouse chromosome 1, with phenotypic effects. Fine-mapping reduced the genomic intervals and gene content, and the introgression of one QTL region back onto the C57BL/6J-Chr 1A/J/NaJ restored the trait. mRNA expression of non-synonymous genes in the introgressed region in the medulla and pons found evidence for differential expression of three genes, the highest of which was apolipoprotein A2, a lipase regulator; the apo a2 peptide fragment (THEQLTPLVR), highly expressed in the liver, was expressed in low amounts in the medulla but did not correlate with trait expression. This work directly demonstrates the impact of elements on mouse chromosome 1 in respiratory rhythmogenesis.


1987 ◽  
Vol 45 (1) ◽  
pp. 52-54 ◽  
Author(s):  
M.F. Seldin ◽  
H.C. Morse, III ◽  
L. D’Hoostelaere ◽  
J.L. Britten ◽  
A.D. Steinberg

Genetics ◽  
2004 ◽  
Vol 169 (2) ◽  
pp. 833-841 ◽  
Author(s):  
Peter M. Kelmenson ◽  
Petko Petkov ◽  
Xiaosong Wang ◽  
David C. Higgins ◽  
Beverly J. Paigen ◽  
...  

Parasitology ◽  
2014 ◽  
Vol 142 (04) ◽  
pp. 566-575
Author(s):  
HARRY NOYES ◽  
JOHN GITHIORI ◽  
JAN E. BRADLEY ◽  
STEVE KEMP ◽  
JERZY M. BEHNKE

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