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Kaneto H Matsuoka TA Nakatani Y Miyatsuka T Matsuhisa M Hori M Yamasaki Y 《The Journal of biological chemistry》2005,280(15):15047-15052
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Insulin is an essential hormone with key roles in energy homeostasis and body composition. Mice and rats, unlike other mammals, have two insulin genes: the rodent-specific Ins1 gene and the ancestral Ins2 gene. The relationships between insulin gene dosage and obesity has previously been explored in male and female Ins2-/- mice with full or reduced Ins1 dosage, as well as in female Ins1-/- mice with full or partial Ins2 dosage. We report herein unexpected hyper-variability in Ins1-null male mice, with respect to their circulating insulin levels and to the physiological effects of modulating Ins2 gene dosage. Two large cohorts of Ins1-/-:Ins2+/- mice and their Ins1-/-:Ins2+/+ littermates were fed chow diet or high fat diet (HFD) from weaning, and housed in specific pathogen-free conditions. Cohort A and cohort B were studied one year apart. Contrary to female mice from the same litters, inactivating one Ins2 allele on the complete Ins1-null background did not consistently cause a reduction of circulating insulin in male mice, on either diet. In cohort A, all HFD-fed males showed an equivalent degree of insulin hypersecretion and weight gain, regardless of Ins2 dosage. In cohort B the effects of HFD appeared generally diminished, and cohort B Ins1-/-:Ins2+/- males showed decreased insulin levels and body mass compared to Ins1-/-:Ins2+/+ littermates, on both diets. Although experimental conditions were consistent between cohorts, we found that HFD-fed Ins1-/-:Ins2+/- mice with lower insulin levels had increased corticosterone. Collectively, these observations highlight the phenotypic characteristics that change in association with differences in circulating insulin and Ins2 gene dosage, particularly in male mice. 相似文献
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Meur G Qian Q da Silva Xavier G Pullen TJ Tsuboi T McKinnon C Fletcher L Tavaré JM Hughes S Johnson P Rutter GA 《The Journal of biological chemistry》2011,286(15):13647-13656
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Yoshikazu Hasegawa Yoko Daitoku Seiya Mizuno Yoko Tanimoto Saori Mizuno-Iijima Miki Matsuo Noriko Kajiwara Masatsugu Ema Hisashi Oishi Yoshihiro Miwa Kazuyuki Mekada Atsushi Yoshiki Satoru Takahashi Fumihiro Sugiyama Ken-ichi Yagami 《Experimental Animals》2014,63(2):183-191
Cre/loxP system-mediated site-specific recombination is utilized to study gene function
in vivo. Successful conditional knockout of genes of interest is
dependent on the availability of Cre-driver mice. We produced and characterized pancreatic
β cell-specific Cre-driver mice for use in diabetes mellitus research. The gene encoding
Cre was inserted into the second exon of mouse Ins1 in a bacterial
artificial chromosome (BAC). Five founder mice were produced by microinjection of
linearized BAC Ins1-cre. The transgene was integrated between
Mafa and the telomere on chromosome 15 in one of the founders, BAC
Ins1-cre25. To investigate Cre-loxP recombination, BAC Ins1-cre25 males were crossed with
two different Cre-reporters, R26R and R26GRR females. On gross observation, reporter
signal after Cre-loxP recombination was detected exclusively in the adult pancreatic
islets in both F1 mice. Immunohistological analysis indicated that Cre-loxP
recombination-mediated reporter signal was colocalized with insulin in pancreatic islet
cells of both F1 mice, but not with glucagon. Moreover, Cre-loxP recombination
signal was already observed in the pancreatic islets at E13.5 in both F1
fetuses. Finally, we investigated ectopic Cre-loxP recombination for
Ins1, because the ortholog Ins2 is also expressed in the
brain, in addition to the pancreas. However, there was no Cre-loxP recombination-mediated
reporter signal in the brain of both F1 mice. Our data suggest that BAC
Ins1-cre25 mice are a useful Cre-driver C57BL/6N for pancreatic β cell-specific Cre-loxP
recombination, except for crossing with knock-in mice carrying floxed gene on chromosome
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IN SITU LOCALIZATION OF GLOBIN MESSENGER RNA FORMATION : I. During Mouse Fetal Liver Development 总被引:9,自引:3,他引:6 下载免费PDF全文
Globin mRNA levels in 11–15-day mouse fetal liver cells have been estimated by in situ hybridization of a highly labeled DNA copy (cDNA) of adult globin messenger RNAs (mRNAs) (globin cDNA) to fixed preparations of cells. Under the conditions employed, no significant in situ hybridization occurred to lymphoma cells (L 51787), mouse L cells, or hepatocytes; whereas reticulocytes from phenyl hydrazine-treated mice showed extensive in situ hybridization. The proportion of fetal liver cells showing predominantly cytoplasmic in situ hybridization increased from about 30% at the 11th day of development to 80–85% by days 13–15. Unlike more mature cells, proerythroblasts did not show in situ hybridization, except to a slight extent at later stages of development. These studies therefore indicate that globin mRNAs begin to accumulate during or shortly after the proerythroblastbasophilic erythroblast transition. The fact that certain immature erythroid cells from 14-day fetal liver contain substantial amounts of globin mRNAs has been confirmed by comparing the hybridization in solution of globin cDNA to cytoplasmic RNA extracted from total fetal liver cells or from immature erythroid cells obtained by treatment of fetal liver cells with an antiserum raised against erythrocytes. 相似文献
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Deltour L Vandamme J Jouvenot Y Duvillié B Kelemen K Schaerly P Jami J Paldi A 《Gene expression patterns : GEP》2004,5(2):297-300
There are two functional insulin genes in the mouse genome. The Ins2 gene is imprinted and expressed monoallelically from the paternal allele in the yolk sac. In the present study we have re-examined the imprinting status of Ins1. We found that Ins1 is not expressed in the yolk sac of several laboratory mouse strains. The asynchrony of replication at the wild type locus was significantly lower than at imprinted loci and was more similar to non-imprinted loci. Finally, we have taken the advantage of the Ins1(neo) allele created by homologous recombination to examine the allelic usage at this locus. We observed that the neo gene inserted at the Ins1 locus was expressed from both the paternally and the maternally transmitted allele. Therefore, the Ins1 gene does not share any of the basic properties of imprinted genes. On the basis of these data, we concluded that Ins1 locus is unlikely to be imprinted in common laboratory mice. 相似文献
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