Development of Dolichos biflorus agglutinin (DBA) binding sites in the bile duct of the embryonic mouse liver

1988 ◽  
Vol 178 (1) ◽  
pp. 15-20 ◽  
Author(s):  
N. Shiojiri ◽  
H. Katayama
Keyword(s):  
Bile Duct ◽  
Binding Sites ◽  
Mouse Liver ◽  
Embryonic Mouse ◽  
Dolichos Biflorus ◽  
Dolichos Biflorus Agglutinin

The crypt cycle in mouse small intestinal epithelium

1994 ◽  
Vol 107 (12) ◽  
pp. 3271-3279 ◽  
Author(s):  
Y.Q. Li ◽  
S.A. Roberts ◽  
U. Paulus ◽  
M. Loeffler ◽  
C.S. Potten
Keyword(s):  
Binding Sites ◽  
Laboratory Mouse ◽  
Subsequent Development ◽  
Fission Process ◽  
Dolichos Biflorus ◽  
Dolichos Biflorus Agglutinin ◽  
Adult Mice ◽  
Crypt Fission ◽  
Small Intestinal ◽  
Peroxidase Conjugate

We have used a mutation-induced marker system in the intestine of mice heterozygous at the Dlb-1 locus, which determines the expression of binding sites for the lectin Dolichos biflorus agglutinin, and the frequency of clustering of mutated crypts with time as a means of investigating the frequency of the crypt fission process and the crypt cycle. Whole-mount preparations from heterozygous Dlb-1b/Dlb-1a mice were stained with a peroxidase conjugate of Dolichos biflorus agglutinin. Mutations at the Dlb-1b locus in crypt stem cells result in loss of DBA-Px binding in these cells and subsequently their progeny, which eventually results in a rare isolated single, unstained crypt. The subsequent development of pairs, triplets and clusters of negative staining crypts has been assumed to be the result of crypt fission. The frequency of these fission events has been measured in control untreated mice. These negative crypts are the result of spontaneous mutations. We have also looked at mutated crypts after treatment with N-nitroso-N-ethylurea or N-methyl-N'-nitro-N-nitrosoguanidine of young adult mice, which elevates the number of mutations. Our results suggest that the crypt cycle in control animals is very long, 187 +/- 44 weeks (3.6 years, i.e. essentially the life of a laboratory mouse). This implies that about a third of the crypts may divide once in the life of a mouse. After sufficient time for conversion of mixed crypts to monophenotypic crypts after mutagen treatment several clusters of negative crypts were seen.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Discrete Distribution of binding sites for Dolichos biflorus agglutinin (DBA) and for peanut agglutinin (PNA) in mouse organ tissues.

1981 ◽  
Vol 29 (7) ◽  
pp. 779-780 ◽  
Author(s):  
M Watanabe ◽  
T Muramatsu ◽  
H Shirane ◽  
K Ugai
Keyword(s):  
Binding Sites ◽  
Cell Lineage ◽  
Discrete Distribution ◽  
Fluorescein Isothiocyanate ◽  
Superficial Layer ◽  
Pancreatic Ducts ◽  
Peanut Agglutinin ◽  
Dolichos Biflorus ◽  
Dolichos Biflorus Agglutinin ◽  
Collecting Tubules

The distribution of binding sites for two lectins with different specificities was studied in adult mice by staining paraffin sections with lectins labeled either with fluorescein isothiocyanate or horseradish peroxidase. Binding sites for Dolichos biflorus agglutinin, a lectin specific to terminal alpha-N-acetylgalactosamine residue, were detected only in several restricted regions, such as collecting tubules and Bowman's capsules of the kidney, bile ducts, pancreatic ducts, sperms, oocytes, some secreting cells, and the secreted mucin itself. Binding sites for peanut agglutinin (PNA), a lectin specific to terminal beta-galactosyl residue, were distributed more widely. However, differentiation-dependent alterations in the expression of PNA binding sites have been observed in two types of cell lineage. During the course of spermatogenesis, the binding sites were expressed at the stage of spermatocytes. In the epithelium of esophagus, the binding sites were present in cells of the superficial layer.

The origin of intrahepatic bile duct cells in the mouse

Development ◽  
1984 ◽  
Vol 79 (1) ◽  
pp. 25-39
Author(s):  
Nobuyoshi Shiojiri
Keyword(s):  
Bile Duct ◽  
Mouse Liver ◽  
Intrahepatic Bile Duct ◽  
Normal Liver ◽  
Liver Parenchyma ◽  
Newborn Mice ◽  
Embryonic Mouse ◽  
Intrahepatic Bile Ducts ◽  
Duct Cells ◽  
Liver Fragments

The origin of the intrahepatic bile ducts in the embryonic mouse liver was investigated. At 12·5 and 13·5 gestation days in the C3H/Tw strain mouse, the liver parenchyma contains morphologically and histochemically homogeneous immature hepatocytes but not bile duct cells. When the liver fragments were cultured in the testis, immature hepatocytes differentiated into large hepatocytes for the most part and also into bile duct cells. In contrast, when the similar liver fragments were cultured under the skin of newborn mice, bile duct cells differentiated much earlier in all transplants than those cultured in the testis. These bile duct cells were considered to be the intrahepatic bile duct cells, since they did not form biliary glands but possessed a basal lamina and histochemical characteristics of intrahepatic bile duct cells of the normal liver. The origin of the endodermal epithelial cells in the mouse liver is discussed with special attention to the differentiation of the intrahepatic bile duct cells from the immature hepatocytes.

scholarly journals The gene controlling the binding sites of Dolichos biflorus agglutinin, Dlb-1, is on chromosome 11 of the mouse

1986 ◽  
Vol 47 (2) ◽  
pp. 125-129 ◽  
Author(s):  
H. G. Uiterdijk ◽  
B. A. J. Ponder ◽  
M. F. W. Festing ◽  
J. Hilgers ◽  
L. Skow ◽  
...  
Keyword(s):  
Intestinal Epithelium ◽  
Vascular Endothelium ◽  
Recombinant Inbred ◽  
Binding Sites ◽  
Inbred Strains ◽  
Recombinant Inbred Strains ◽  
Binding Pattern ◽  
Chromosome 11 ◽  
Dolichos Biflorus ◽  
Dolichos Biflorus Agglutinin

SUMMARYA locus, Dlb-1, controlling the binding of the lectin from Dolichos biflorus to the intestinal epithelium and vascular endothelium of mice has been located on chromosome 11, 3.1 ± 1.4 centimorgans proximal to Rex, using recombinant inbred strains and conventional backcrosses with three-point linkage tests.The two alleles so far discovered at this locus behave unusually. The Dlb-1a allele causes binding to the vascular endothelium but not to the intestinal epithelium while Dlb-1b induces the exact reciprocal binding pattern, and the heterozygote shows both patterns.

Lowered antioxidant enzymes in spontaneously transformed embryonic mouse liver cells in culture

1993 ◽  
Vol 14 (7) ◽  
pp. 1457-1463 ◽  
Author(s):  
Yi Sun ◽  
Larry W. Oberley ◽  
Terry D. Oberley ◽  
James H. Elwell ◽  
Elaine Sierra-Rivera
Keyword(s):  
Antioxidant Enzymes ◽  
Mouse Liver ◽  
Liver Cells ◽  
Embryonic Mouse ◽  
Cells In Culture

scholarly journals Evolution of mouse circadian enhancers from transposable elements

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Julius Judd ◽  
Hayley Sanderson ◽  
Cédric Feschotte
Keyword(s):  
Gene Expression ◽  
Transposable Elements ◽  
Binding Sites ◽  
Mouse Liver ◽  
Integration Site ◽  
Point Mutations ◽  
Regulatory Elements ◽  
Circadian Gene ◽  
Binding Motifs ◽  
Reporter Assays

Abstract Background Transposable elements are increasingly recognized as a source of cis-regulatory variation. Previous studies have revealed that transposons are often bound by transcription factors and some have been co-opted into functional enhancers regulating host gene expression. However, the process by which transposons mature into complex regulatory elements, like enhancers, remains poorly understood. To investigate this process, we examined the contribution of transposons to the cis-regulatory network controlling circadian gene expression in the mouse liver, a well-characterized network serving an important physiological function. Results ChIP-seq analyses reveal that transposons and other repeats contribute ~ 14% of the binding sites for core circadian regulators (CRs) including BMAL1, CLOCK, PER1/2, and CRY1/2, in the mouse liver. RSINE1, an abundant murine-specific SINE, is the only transposon family enriched for CR binding sites across all datasets. Sequence analyses and reporter assays reveal that the circadian regulatory activity of RSINE1 stems from the presence of imperfect CR binding motifs in the ancestral RSINE1 sequence. These motifs matured into canonical motifs through point mutations after transposition. Furthermore, maturation occurred preferentially within elements inserted in the proximity of ancestral CR binding sites. RSINE1 also acquired motifs that recruit nuclear receptors known to cooperate with CRs to regulate circadian gene expression specifically in the liver. Conclusions Our results suggest that the birth of enhancers from transposons is predicated both by the sequence of the transposon and by the cis-regulatory landscape surrounding their genomic integration site.

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