Chromosomal assignments of 23 biochemical loci of the rat by using rat × mouse somatic cell hybrids

Yasue, M.; Serikawa, Tadao; Yamada, Junzo

doi:10.1159/000133133

Cited by 52 publications

(12 citation statements)

References 20 publications

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“…A panel of 18 ratimouse SCHs [32] was kindly made available to us by Professor T. Serikawa (Institute of Laboratory Animals, Kyoto University, Kyoto, Japan). From the rat and mouse fetuin-B cDNAs (see the Results section), an oligonucleotide pair that would favour an amplification of the corresponding rat cDNA was designed with the following conditions : amplified area to be located in the 3h-non-coding sequence of the cDNAs ; a 100 % match between the oligonucleotides and the rat cDNA ; a high number of mismatches in each oligonucleotides versus the mouse fetuin-B cDNA ; amplicon size in the 200-bp range ; and T m in the 56-60 mC range.…”

Section: Rat Gene Assignment With a Panel Of Ratimouse Somatic Cell Hmentioning

confidence: 99%

“…This allowed for chromosomal assignment of the rat fetuin-B gene from a panel of 18 ratimouse SCHs. Indeed, the distributions of rat chromosomes in these 18 hybrids [32] versus the distribution of a rat fetuin-B gene amplicon in the same hybrids (Table 3) allowed us to assign the fetuin-B gene to Rattus nor egicus chromosome 4 (RNO4).…”

Section: Table 1 Hepatic Levels Of Fetuin-a and Fetuin-b Mrnas As A Fmentioning

confidence: 99%

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Fetuin-B, a second member of the fetuin family in mammals

Olivier

Soury

Ruminy

et al. 2000

Biochemical Journal

112

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A set of orthologous plasma proteins found in human, sheep, pig, cow and rodents, now collectively designated fetuin-A, constitutes the fetuin family. Fetuin-A has been identified as a major protein during fetal life and is also involved in important functions such as inhibition of the insulin receptor tyrosine kinase activity, protease inhibitory activities and development-associated regulation of calcium metabolism and osteogenesis. Furthermore, fetuin-A is a key partner in the recovery phase of an acute inflammatory response. We now describe a second protein of the fetuin family, called fetuin-B, which is found at least in human and rodents. On grounds of domain homology, overall conservation of cysteine residues and chromosomal assignments of the corresponding genes in these species, fetuin-B is unambiguously a paralogue of fetuin-A. Yet, fetuin-A and fetuin-B exhibit significant differences at the amino acid sequence level, notably including variations with respect to the archetypal fetuin-specific signature. Differences and similarities in terms of gene regulation were also observed. Indeed, studies performed during development in rat and mouse showed for the first time high expression of a member of the fetuin family in adulthood, as shown with the fetuin-B mRNA in rat. However, like its fetuin-A counterpart, the fetuin-B mRNA level is down-regulated during the acute phase of experimentally induced inflammation in rat.

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Section: Rat Gene Assignment With a Panel Of Ratimouse Somatic Cell Hmentioning

confidence: 99%

Section: Table 1 Hepatic Levels Of Fetuin-a and Fetuin-b Mrnas As A Fmentioning

confidence: 99%

Fetuin-B, a second member of the fetuin family in mammals

Olivier

Soury

Ruminy

et al. 2000

Biochemical Journal

112

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“…1991). Karyotype and isozyme analyses to determine the rat chromosome content of the hybrid cell lines were carried out on the cells from which the DNAs were prepared (Yasue et al, 1991).…”

Section: Methodsmentioning

confidence: 99%

Chromosomal assignments of the genes for the calcineurin Aα (Calna1) and Aβ subunits (Calna2) in the rat

Yamada

Kim

Muramatsu

et al. 1994

Cytogenet Genome Res

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“…In the light of the more precise map position of Tscc1 determined in this study, one of the candidate genes for Tscc1 is NQO1 (the gene for quinone oxidoreductase, synonymous with DT-diaphorase or NADH-cytochrome b 5 reductase). 17,18) Quinone oxidoreductase is one of the major enzymes that converts 4NQO to the more active metabolite, 4-hydroxyaminoquinoline 1-oxide (4HAQO). 19,20) Our preliminary study showed that the enzyme activity is higher in DA than in WF rats.…”

Section: )mentioning

confidence: 99%

Five Quantitative Trait Loci Affecting 4‐Nitroquinoline 1‐Oxide‐induced Tongue Cancer in the Rat

Tanuma

Fujii

Hirano

et al. 2001

Japanese Journal of Cancer Research

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In our previous study, Dark-Agouti (DA) rats were found to be highly susceptible to 4-nitroquinoline 1-oxide (4NQO)-induced tongue carcinoma (TC), whereas Wistar/Furth (WF) rats were barely susceptible. Interval mapping analysis of reciprocal backcross rats showed two quantitative trait loci (QTL) on rat chromosomes (RNO) 1 and 19. In the present study, a composite interval mapping analysis was applied to 4NQO-induced TC in 130 (DA × × × ×WF) F2 rats, demonstrating five independent QTL, Tongue squamous cell carcinoma 1-5 (Tscc1-5), responsible for phenotypic differences in the size and number of TCs in the two strains. Two of these QTL were mapped on RNO1, and the others were mapped on RNO4, 14, and 19. The DA allele at these loci consistently yielded semidominant susceptibility to TC. Out of the five loci detected in this F2 generation, Tscc1 and 2 were identical to Stc1 and Rtc1 described in our previous study, but the other three were novel. We propose a new nomenclature consistent with their function. Genome-wide screening of the F2 progeny also suggested the presence of three additional QTL on RNO5, 6, and 10. The possible roles of these loci in tongue carcinogenesis are discussed. Key words: Genetic susceptibility -QTL -Tongue cancer -Rat -4-Nitroquinoline 1-oxideTongue carcinoma (TC) is one of the most frequent malignancies in the head and neck region. An increase in TC has been reported in the Western world over the past ten years. TC has a poor prognosis because therapeutic strategies provide limited effects.1-4) For effective prevention of TC, it would be necessary to identify the genetically predisposed risk group. However, virtually nothing is known about the genetic predisposition to TC.Recently, we found that the Dark-Agouti (DA) strain of rats had an extremely high susceptibility to 4-nitroquinoline 1-oxide (4NQO)-induced squamous cell carcinoma of the tongue. Virtually 100% of DA rats given drinking water containing 0.001% 4NQO developed one or more large TC within 180 days of administration, whereas the Wistar/Furth (WF) strain of rats was much less susceptible. [5][6][7][8] In the previous study with reciprocal backcrosses between DA and WF rats, 7,8) DA rats were shown to have a semidominant susceptibility locus, Stc1 (Susceptibility to TC-1) on rat chromosome (RNO) 19, and WF rats, another semidominant resistance gene Rtc1 (Resistance to TC-1) on RNO1.In this study, to scrutinize further the genetic predisposition to TC in the rat, we studied F2 progeny between DA and WF strains by means of a composite interval mapping analysis. After several statistical trials, we employed a quantitative parameter for tumor number, TC >3 mm in diameter, rather than TC >5 mm. In addition to two quantitative trait loci (QTL) described in the previous study, three novel QTL have been found to affect TC susceptibility. These five QTL explain almost all phenotypic variations between the two strains. MATERIALS AND METHODS Animals and phenotypeThe origin of DA rats is related to Copenhagen rats, although there is n...

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Chromosomal assignments of 23 biochemical loci of the rat by using rat × mouse somatic cell hybrids

Cited by 52 publications

References 20 publications

Fetuin-B, a second member of the fetuin family in mammals

Fetuin-B, a second member of the fetuin family in mammals

Chromosomal assignments of the genes for the calcineurin Aα (<i>Calna</i><i>1</i>) and Aβ subunits (<i>Calna2</i>) in the rat

Five Quantitative Trait Loci Affecting 4‐Nitroquinoline 1‐Oxide‐induced Tongue Cancer in the Rat

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