Assignment of the gene coding for HPRT enzyme to Syrian hamster X Chromosome by microcell fusion

1995 ◽  
Vol 6 (2) ◽  
pp. 152-153 ◽  
Author(s):  
K. Islam ◽  
M. Q. Islam ◽  
G. Levan
Keyword(s):  
X Chromosome ◽  
Syrian Hamster ◽  
Gene Coding ◽  
Microcell Fusion

scholarly journals Structure of amplified DNA in different Syrian hamster cell lines resistant to N-(phosphonacetyl)-L-aspartate.

1983 ◽  
Vol 3 (11) ◽  
pp. 2076-2088 ◽  
Author(s):  
F Ardeshir ◽  
E Giulotto ◽  
J Zieg ◽  
O Brison ◽  
W S Liao ◽  
...  
Keyword(s):  
Cell Line ◽  
Cell Lines ◽  
Syrian Hamster ◽  
Mutant Cell ◽  
Screening Method ◽  
Wild Type ◽  
Mutant Cell Line ◽  
Gene Coding ◽  
Cad Gene ◽  
Mutant Cells

Syrian hamster cell lines selected in multiple steps for resistance to high levels of N-(phosphonacetyl)-L-aspartate (PALA) contain many copies of the gene coding for the pyrimidine pathway enzyme CAD. Approximately 500 kilobases of additional DNA was coamplified with each copy of the CAD gene in several cell lines. To investigate its structure and organization, we cloned ca. 162 kilobases of coamplified DNA from cell line 165-28 and ca. 68 kilobases from cell line B5-4, using a screening method based solely on the greater abundance of amplified sequences in the resistant cells. Individual cloned fragments were then used to probe Southern transfers of genomic DNA from 12 different PALA-resistant mutants and the wild-type parents. A contiguous region of DNA ca. 44 kilobases long which included the CAD gene was amplified in all 12 mutants. However, the fragments cloned from 165-28 which were external to this region were not amplified in any other mutant, and the external fragments cloned from B5-4 were not amplified in two of the mutants. These results suggest that movement or major rearrangement of DNA may have accompanied some of the amplification events. We also found that different fragments were amplified to different degrees within a single mutant cell line. We conclude that the amplified DNA was not comprised of identical, tandemly arranged units. Its structure was much more complex and was different in different mutants. Several restriction fragments containing amplified sequences were found only in the DNA of the mutant cell line from which they were isolated and were not detected in DNA from wild-type cells or from any other mutant cells. These fragments contained novel joints created by rearrangement of the DNA during amplification. The cloned novel fragments hybridized only to normal fragments in every cell line examined, except for the line from which each novel fragment was isolated or the parental population for that line. This result argues that "hot spots" for forming novel joints are rare or nonexistent.

Structure of amplified DNA in different Syrian hamster cell lines resistant to N-(phosphonacetyl)-L-aspartate

1983 ◽  
Vol 3 (11) ◽  
pp. 2076-2088
Author(s):  
F Ardeshir ◽  
E Giulotto ◽  
J Zieg ◽  
O Brison ◽  
W S Liao ◽  
...  
Keyword(s):  
Cell Line ◽  
Cell Lines ◽  
Syrian Hamster ◽  
Mutant Cell ◽  
Screening Method ◽  
Wild Type ◽  
Mutant Cell Line ◽  
Gene Coding ◽  
Cad Gene ◽  
Mutant Cells

Syrian hamster cell lines selected in multiple steps for resistance to high levels of N-(phosphonacetyl)-L-aspartate (PALA) contain many copies of the gene coding for the pyrimidine pathway enzyme CAD. Approximately 500 kilobases of additional DNA was coamplified with each copy of the CAD gene in several cell lines. To investigate its structure and organization, we cloned ca. 162 kilobases of coamplified DNA from cell line 165-28 and ca. 68 kilobases from cell line B5-4, using a screening method based solely on the greater abundance of amplified sequences in the resistant cells. Individual cloned fragments were then used to probe Southern transfers of genomic DNA from 12 different PALA-resistant mutants and the wild-type parents. A contiguous region of DNA ca. 44 kilobases long which included the CAD gene was amplified in all 12 mutants. However, the fragments cloned from 165-28 which were external to this region were not amplified in any other mutant, and the external fragments cloned from B5-4 were not amplified in two of the mutants. These results suggest that movement or major rearrangement of DNA may have accompanied some of the amplification events. We also found that different fragments were amplified to different degrees within a single mutant cell line. We conclude that the amplified DNA was not comprised of identical, tandemly arranged units. Its structure was much more complex and was different in different mutants. Several restriction fragments containing amplified sequences were found only in the DNA of the mutant cell line from which they were isolated and were not detected in DNA from wild-type cells or from any other mutant cells. These fragments contained novel joints created by rearrangement of the DNA during amplification. The cloned novel fragments hybridized only to normal fragments in every cell line examined, except for the line from which each novel fragment was isolated or the parental population for that line. This result argues that "hot spots" for forming novel joints are rare or nonexistent.

Structure and Localization on the X Chromosome of the Gene Coding for the Human Filopodial Protein Moesin (MSN)

Genomics ◽  
1994 ◽  
Vol 19 (2) ◽  
pp. 326-333 ◽  
Author(s):  
K.K. Wilgenbus ◽  
C.-L. Hsieh ◽  
W.T. Lankes ◽  
A. Milatovich ◽  
U. Francke ◽  
...  
Keyword(s):  
X Chromosome ◽  
Gene Coding

The gene coding the human S11 surface antigens maps between the loci for HPRT and G6PD on the X-chromosome

1983 ◽  
Vol 149 (2) ◽  
pp. 325-334 ◽  
Author(s):  
Michael E. Kamarck ◽  
Catherine A. Macyko ◽  
Ann C. Cunningham ◽  
Frank H. Ruddle
Keyword(s):  
X Chromosome ◽  
Surface Antigens ◽  
Gene Coding

Banded aggregates containing fibrillin are present in the cartilage matrix adjacent to chondrocytes in individuals affected with scoliosis

1992 ◽  
Vol 50 (1) ◽  
pp. 892-893
Author(s):  
Douglas R. Keene ◽  
Magaret Fairhurst ◽  
Catherine C. Ridgway ◽  
Lynn Y. Sakai
Keyword(s):  
Connective Tissue ◽  
Marfan Syndrome ◽  
Cross Section ◽  
Immunoelectron Microscopy ◽  
Cartilage Matrix ◽  
Negative Stain ◽  
Gene Coding ◽  
Rotary Shadowing

Matrix microfibrils are present in the connective tissue matrices of all tissues. Following standard TEM processing, they appear in cross section as cylindrical fibrils 8-10 nm in diameter, often associated with amorphous elastin. They are also seen in the absence of amorphous elastin, for example in the shallow papillary layer of skin, and also in cartilage matrix (Figure 1). Negative stain and rotary shadowing studies suggest that microfibrils are composed of laterally associated globular structures connected by fine filamentous strands (“ beaded strings”), and that they are extendable. Immunoelectron microscopy has demonstrated that fibrillin, a 350 Kd glycoprotein, is distributed along all microfibrils with a relaxed periodicity of about 54 nm The gene coding for fibrillin has recently been identified and is defective in the Marfan syndrome.

Effect of intestinal alkalinization on irinotecan (CPT-11)-induced diarrhea in the golden Syrian hamster model

2001 ◽  
Vol 120 (5) ◽  
pp. A613-A613
Author(s):  
T IKEGAMI ◽  
P LATHAM ◽  
K KOBAYASHI ◽  
K ARIMORI ◽  
B BOUSCAREL
Keyword(s):  
Syrian Hamster ◽  
Hamster Model ◽  
Golden Syrian Hamster
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