Localization of the active gene of aldolase on chromosome 16, and two aldolase A pseudogenes on chromosomes 3 and 10

1988 ◽  
Vol 78 (2) ◽  
pp. 167-174 ◽  
Author(s):  
S. Serero ◽  
P. Maire ◽  
Nguyen Van Cong ◽  
O. Cohen-Haguenauer ◽  
M. S. Gross ◽  
...  
Keyword(s):  
Chromosome 16 ◽  
Active Gene ◽  
Aldolase A

Molecular gene mapping of human aldolase A (ALDOA) gene to chromosome 16

1987 ◽  
Vol 76 (1) ◽  
Author(s):  
A. Kukita ◽  
M.C. Yoshida ◽  
S. Fukushige ◽  
M. Sakakibara ◽  
K. Joh ◽  
...  
Keyword(s):  
Gene Mapping ◽  
Chromosome 16 ◽  
Aldolase A

scholarly journals Novobiocin induces the in vivo cleavage of active gene sequences in intact cells.

1986 ◽  
Vol 261 (22) ◽  
pp. 10359-10365
Author(s):  
B Villeponteau ◽  
T M Pribyl ◽  
M H Grant ◽  
H G Martinson
Keyword(s):  
Gene Sequences ◽  
Intact Cells ◽  
Active Gene

Congenic strains confirm aerobic running capacity quantitative trait loci on rat chromosome 16 and identify possible intermediate phenotypes

2007 ◽  
Vol 29 (1) ◽  
pp. 91-97 ◽  
Author(s):  
Justin A. Ways ◽  
Brian M. Smith ◽  
John C. Barbato ◽  
Ramona S. Ramdath ◽  
Krista M. Pettee ◽  
...  
Keyword(s):  
Quantitative Trait Loci ◽  
Quantitative Trait ◽  
Strain Differences ◽  
Proximal Portion ◽  
Chromosome 16 ◽  
Rat Strains ◽  
High Performing ◽  
Intermediate Phenotypes ◽  
Trait Loci ◽  
Inbred Rat

We previously identified two inbred rat strains divergent for treadmill aerobic running capacity (ARC), the low-performing Copenhagen (COP) and the high-performing DA rats, and used an F2(COP×DA) population to identify ARC quantitative trait loci (QTLs) on rat chromosome 16 (RNO16) and the proximal portion of rat chromosome 3 (RNO3). Two congenic rat strains were bred to further investigate these ARC QTLs by introgressing RNO16 and the proximal portion of RNO3 from DA rats into the genetic background of COP rats and were named COP.DA(chr 16) and COP.DA(chr 3), respectively. COP.DA(chr 16) rats had significantly greater ARC compared with COP rats (696.7 ± 38.2 m vs. 571.9 ± 27.5 m, P = 0.03). COP.DA(chr 3) rats had increased, although not significant, ARC compared with COP rats (643.6 ± 40.9 m vs. 571.9 ± 27.5 m). COP.DA(chr 16) rats had significantly greater subcutaneous abdominal fat, as well as decreased fasting triglyceride levels, compared with COP rats ( P < 0.05), indicating that genes responsible for strain differences in fat metabolism are also located on RNO16. While this colocalization of QTLs may be coincidental, it is also possible that these differences in energy balance may be associated with the superior running performance of COP.DA(chr 16) consomic rats.

scholarly journals An opportunistic promoter sharing regulatory sequences with either a muscle-specific or a ubiquitous promoter in the human aldolase A gene.

1993 ◽  
Vol 13 (1) ◽  
pp. 9-17 ◽  
Author(s):  
J P Concordet ◽  
M Salminen ◽  
J Demignon ◽  
C Moch ◽  
P Maire ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Integration Site ◽  
Regulatory Elements ◽  
Regulatory Sequences ◽  
Beta Globin ◽  
Fast Skeletal Muscle ◽  
High Level Expression ◽  
Adult Skeletal Muscle ◽  
High Level ◽  
Aldolase A

The human aldolase A gene is transcribed from three different promoters, pN, pM, and pH, all of which are clustered within a small 1.6-kbp DNA domain. pM, which is highly specific to adult skeletal muscle, lies in between pN and pH, which are ubiquitous but particularly active in heart and skeletal muscle. A ubiquitous enhancer, located just upstream of pH start sites, is necessary for the activity of both pH and pN in transient transfection assays. Using transgenic mice, we studied the sequence controlling the muscle-specific promoter pM and the relations between the three promoters and the ubiquitous enhancer. A 4.3-kbp fragment containing the three promoters and the ubiquitous enhancer showed an expression pattern consistent with that known in humans. In addition, while pH was active in both fast and slow skeletal muscles, pM was active only in fast muscle. pM activity was unaltered by the deletion of a 1.8-kbp region containing the ubiquitous enhancer and the pH promoter, whereas pN remained active only in fast skeletal muscle. These findings suggest that in fast skeletal muscle, a tissue-specific enhancer was acting on both pN and pM, whereas in other tissues, the ubiquitous enhancer was necessary for pN activity. Finally, a 2.6-kbp region containing the ubiquitous enhancer and only the pH promoter was sufficient to bring about high-level expression of pH in cardiac and skeletal muscle. Thus, while pH and pM function independently of each other, pN, remarkably, shares regulatory elements with each of them, depending on the tissue. Importantly, expression of the transgenes was independent of the integration site, as originally described for transgenes containing the beta-globin locus control region.

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