Murine complement component 3: genetic variation and linkage to H-2.

Silva, F P Da; Hoecker, G; Day, Noorbibi K.; Vienne, K; Rubinstein, Pablo

doi:10.1073/pnas.75.2.963

Cited by 66 publications

(11 citation statements)

References 24 publications

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“…The recombination rates between these loci are consistent with previous estimates of the position of these genes on chromosome 17 (14,(16)(17)(18). The MHC haplotype provided the best correlation with disease (9.9% discordance with disease phenotype).…”

Section: Resultssupporting

confidence: 78%

Genetic analysis of the imperfect association of H-2 haplotype with lupus-like autoimmune disease.

Babcock

Appel

Schiff

et al. 1989

Proc. Natl. Acad. Sci. U.S.A.

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Proteinuria, an indicator of renal disease, was evaluated monthly by using tetrabromphenol paper, and was graded 0-3+. Trace proteinuria is <30 mg/dl, 1+ detects 30 mg/dl, 2+ detects 100 mg/dl, and 3+ detects >500 mg/dl. Severe proteinuria was defined as >2+, and animals with this level of proteinuria at 11 months of age or earlier were classified as having severe renal disease (2, 8). These mice usually died from renal failure within 4-8 weeks after development of severe proteinuria. Animals with negative or trace proteinuria at 12 months of age were classified as having no evidence of renal disease.Southern Analysis of Genomic DNA. Liver and kidney DNA from each animal was isolated as described (9). DNA (10 pkg) was digested with restriction enzymes at a concentration of 2 units per ,ug of DNA for 1 hr at 370C. This procedure was repeated once. Various enzymes were utilized depending on the probe used: Pvu II for I-Aa, BamHI for C3, Pvu II for TU66, and Bgl II for both TU169 and the a-globin pseudogene 4 (a-q4). Digested DNAs were subjected to electrophoresis through agarose gels (10). A 0.7% gel was used for MHC, TU66, TU169, and a-+4, and the gels were run for 20 hr. To separate the fragments hybridizing to the C3 probe, a 1.5% gel was run for 48 hr. The DNA was transferred to nitrocellulose filters, baked, and hybridized with a 32p labeled probe as described (10), except that the depurination step was omitted and the gel was irradiated for 7 min with shortwave UV light before denaturation to facilitate transfer ofDNA to nitrocellulose (11). Hybridized filters were washed in 2x SSC/1% SDS at room temperature followed by 0.1X SSC/1% SDS at 550C for 45 min (lx SSC = 0.15 M Abbreviation: MHC, major histocompatibility complex.fTo whom reprint requests should be addressed. 7552The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

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Section: Resultssupporting

confidence: 78%

Genetic analysis of the imperfect association of H-2 haplotype with lupus-like autoimmune disease.

Babcock

Appel

Schiff

et al. 1989

Proc. Natl. Acad. Sci. U.S.A.

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“…Included within the H-2 complex is a gene that controls the level of a serum protein (Ss). Recently, a gene controlling an electrophoretic variant of murine C3 has been found to be linked to H-2 with a recombination frequency of Chromosome-1 Location of Sas 1 Locus 319 12% (DaSilva et al 1978). Thus, Sas-1 may be the Chromosome 1 equivalent of the Ss locus or of the gene controlling C3.…”

Section: Resultsmentioning

confidence: 94%

Location of theSas-1 locus on mouse chromosome 1

et al. 1978

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Using three sets of recombinant inbred strains (BXD, BXH, and BXJ), we found the locus controlling an antigenic substance (Sas}-1) in murine serum to be closely linked to the Chromosome-1 marker,Dip-1. This linkage was confirmed by an analysis of backcross linkage. The BXD and backcross data suggest that the gene order isId-1-Dip-1-Sas-1-Mls. Data from the three sets of RI strains and the 32 backcross mice lead to the estimate that the recombination frequency betweenDip-1 andSas-1 is 0.030 ±0.015.

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“…It should thus be possible to map these genes. Examination of the pattern of secretion of the hybrid clones (Table 3) shows that production of each of the three rat serum proteins is lost independently of the others, suggesting that the corresponding structural genes are located on separate chromosomes [this is also the situation in the mouse (17)(18)(19)]. Moreover, because these hybrids were selected and propagated in a medium that selects for the presence of an active X chromosome contributed by the rat hepatocyte (the parental mouse hepatoma cells are hypoxanthine phosphoribosyltransferase negative), it is very likely that none of these genes is X linked.…”

Section: Isolation Of Interspeciesmentioning

confidence: 99%

Control of serum protein production in hepatocyte hybridomas: immortalization and expression of normal hepatocyte genes.

Szpirer¹,

Szpirer²,

Wanson³

1980

Proc. Natl. Acad. Sci. U.S.A.

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ABSTRACT"Hepatocyte hybridomas" have been isolated after fusion of adult hepatocytes and a-fetoprotein (AFP-producing mouse hepatoma cells. The yield of viable hybrid clones was low but could be increased by culturing the cells in the presence of insulin. On the basis of their chromosome constitution, the hybrids were classified into two groups characterized by either a single or a double set of mouse (hepatoma) chromosomes. The hybrids segregated rat chromosomes and thus constitute an excellent material for gene mapping studies in the rat.Most of the hepatocyte hybridomas retained the production of one or more rat serum proteins, indicating that the corresponding structural genes, contributed by the normal hepatocyte parent, have been immortalized and maintained in the active state after fusion. However, these hybrids do not produce rat AFP, although mouse AFP synthesis is maintained. This result strongly suggests that silent rat (hepatocyte) AFP genes coexist in hepatocyte hybridoma nuclei with active mouse (hepatoma) AFP genes. Finally, on the basis of certain proerties of these hepatocyte-hepatoma hybrids, we suggest that the nondividing state of the hepatocytes is actively controlled by a regulatory mechanism which prevents DNA synthesis or entry into mitosis or both. Hybrids formed between normal diploid cells and tumor cells of the same tissue origin (hybridomas) have proved useful for immortalizing certain functions expressed by normal differentiated cells, as shown by the numerous studies on the now classical "lymphocyte hybridomas" (1, 2). We have explored the possibility that differentiated liver functions could be immortalized by hybridization of normal hepatocytes with mouse hepatoma cells. In this communication, we report the successful isolation of interspecies "hepatocyte hybridomas" and show that these hybrids provide a tool for immortalizing normal liver functions.Hybridomas could also be valuable for analyzing the expression of differentiated functions subjected to developmental controls or to alterations associated with a malignant phenotype. This possibility has not yet been subjected to much investigation. Production of a-fetoprotein (AFP) is modulated during hepatic differentiation: AFP is produced actively by the fetal hepatocytes but only in trace amounts by the adult liver; and, in addition, it is synthesized by most hepatomas (3, 4). By fusing liver cells which differ in the expression of the AFP gene, it should be possible to explore the mechanisms controlling the expression of this gene. In previous studies, we have shown that hybrids formed between AFP-producing mouse hepatoma cells and non-AFP-producing rat hepatoma cells retain the capacity to secrete mouse AFP (5), unlike hybrids generated between AFP-producing mouse hepatoma cells and fibroblasts (6, 7). By fusing AFP-producing mouse hepatoma cells with adult ratThe publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U....

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Murine complement component 3: genetic variation and linkage to H-2.

Cited by 66 publications

References 24 publications

Genetic analysis of the imperfect association of H-2 haplotype with lupus-like autoimmune disease.

Genetic analysis of the imperfect association of H-2 haplotype with lupus-like autoimmune disease.

Location of theSas-1 locus on mouse chromosome 1

Control of serum protein production in hepatocyte hybridomas: immortalization and expression of normal hepatocyte genes.

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