Regional localization of the fibronectin and gamma crystallin genes to mouse chromosome 1 by in situ hybridization

1988 ◽  
Vol 48 (4) ◽  
pp. 238-241 ◽  
Author(s):  
S.M. Zneimer ◽  
J.E. Womack
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.


2000 ◽  
Vol 89 (3-4) ◽  
pp. 216-217
Author(s):  
C. Popovici ◽  
M.-G. Mattéi ◽  
J.B. Rattner ◽  
D. Birnbaum ◽  
M.-J. Pébusque

Genome ◽  
2011 ◽  
Vol 54 (3) ◽  
pp. 184-195 ◽  
Author(s):  
Robert T. Gaeta ◽  
Tatiana V. Danilova ◽  
Changzeng Zhao ◽  
Rick E. Masonbrink ◽  
Morgan E. McCaw ◽  
...  

Maize-engineered minichromosomes are easily recovered from telomere-truncated B chromosomes but are rarely recovered from A chromosomes. B chromosomes lack known genes, and their truncation products are tolerated and transmitted during meiosis. In contrast, deficiency gametes resulting from truncated A chromosomes prevent their transmission. We report here a de novo compensating translocation that permitted recovery of a large truncation of chromosome 1 in maize. The truncation (trunc-1) and translocation with chromosome 6 (super-6) occurred during telomere-mediated truncation experiments and were characterized using single-gene fluorescent in situ hybridization (FISH) probes. The truncation contained a transgene signal near the end of the broken chromosome and transmitted together with the compensating translocation as a heterozygote to approximately 41%–55% of progeny. Transmission as an addition chromosome occurred in ~15% of progeny. Neither chromosome transmitted through pollen. Transgene expression (Bar) cosegregated with trunc-1 transcriptionally and phenotypically. Meiosis in T1 plants revealed eight bivalents and one tetravalent chain composed of chromosome 1, trunc-1, chromosome 6, and super-6 in diplotene and diakinesis. Our data suggest that de novo compensating translocations allow recovery of truncated A chromosomes by compensating deficiency in female gametes and by affecting chromosome pairing and segregation. The truncated chromosome can be maintained as an extra chromosome or together with the super-6 as a heterozygote.


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

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