scholarly journals ALTERATION OF HISTONES FROM MOUSE EPIDERMAL CELLS AFTER INCUBATION WITH ELASTASE AND HYALURONIDASE

1971 ◽  
Vol 19 (3) ◽  
pp. 182-185 ◽  
Author(s):  
ALVIN SEGAL ◽  
MARGARET SCHROEDER ◽  
BENJAMIN L. VAN DUUREN
Keyword(s):  
Mouse Liver ◽  
Mouse Skin ◽  
Analytical Techniques ◽  
Epidermal Cells ◽  
Ultraviolet Absorption Spectrum ◽  
Tissue Preparation ◽  
Standard Procedures ◽  
Highly Sensitive ◽  
Mammalian Tissues ◽  
Liver Chromatin

Chromatin was isolated from whole mouse skin, mouse epidermal cells and mouse liver by standard procedures used for isolation of chromatin from other mammalian tissues. Chromatin from whole mouse skin or from mouse epidermal cells had not been isolated or characterized earlier. For the preparation of chromatin from mouse epidermal cells, the latter was separated from dermis by incubation for 30 min at 37°C in a solution containing the enzymes elastase and hyaluronidase. The relative proportions of the chromatin components, the T m and the ultraviolet absorption spectrum were all similar to that of chromatin from whole mouse skin which was not treated with enzymes and to other mammalian chromatin preparations. Electrophoresis of the histones from epidermal chromatin in polyacrylamide gels revealed the absence of histones F1, F3 and F2a2 and the appearance of a new band. Histones isolated from chromatin prepared from the whole mouse skin had a gel electrophoresis pattern virtually identical with histones isolated from mouse liver chromatin and to reported histone patterns from other mammalian tissues. The alterations in mouse epidermal histones are similar to reported changes in histones from calf thymus nucleohistone previously subjected to incubation at various temperatures. The enzymatic incubation technique can therefore not be used as a method of isolating unaltered mouse epidermal chromatin. The findings illustrate that very subtle chemical alterations can be induced by usual methods of tissue preparation and that these changes can only be detected by highly sensitive analytical techniques.

scholarly journals Nucleosome distribution on the Jkand Ckimmunoglobulin gene segments of mouse liver chromatin

1983 ◽  
Vol 11 (11) ◽  
pp. 3613-3630 ◽  
Author(s):  
Wolfgang O. Weischet ◽  
Boris O. Glotov ◽  
Hans G. Zachau
Keyword(s):  
Mouse Liver ◽  
Liver Chromatin

scholarly journals Effect of mechanical pressure on c-fos and on the mitotic activity of epidermal cells.

1996 ◽  
Vol 43 (4) ◽  
pp. 593-601
Author(s):  
R Tsanev ◽  
J Yaneva ◽  
K Vaptzarova ◽  
D Markov
Keyword(s):  
Mitotic Cycle ◽  
Mouse Skin ◽  
State Level ◽  
Cellular Membrane ◽  
Camp Level ◽  
Epidermal Cells ◽  
Steady State Level ◽  
Camp Concentration ◽  
Mechanical Pressure ◽  
Two Peaks

A dosed mechanical pressure of 12.5 kg/cm2 applied for 1 min on depilated mouse skin did not cause cellular death or visible alterations of the cellular ultrastructures. However, it had a strong effect on the mitotic cycle of the epidermal cells-stimulating the cells to enter the mitotic cycle and temporarily blocking the G1-->S transition. This effect was strictly limited to the pressed area of the skin. The proto-oncogene c-fos was induced within the first 2 min following application of the pressure. The level of c-fos mRNA showed two peaks during the next 24 h. The first slight peak was preceded by a rapid increase in the cAMP level in the pressed skin, the second-by a fall in the cAMP concentration. A model is suggested to explain the observed effects by reversible functional damage of the cellular membrane affecting the enzymes maintaining the steady state level of cAMP.

scholarly journals Genome-wide analysis of SREBP-1 binding in mouse liver chromatin reveals a preference for promoter proximal binding to a new motif

2009 ◽  
Vol 106 (33) ◽  
pp. 13765-13769 ◽  
Author(s):  
Y.-K. Seo ◽  
H. K. Chong ◽  
A. M. Infante ◽  
S.-S. Im ◽  
X. Xie ◽  
...  
Keyword(s):  
Mouse Liver ◽  
Genome Wide Analysis ◽  
Genome Wide ◽  
Liver Chromatin

Age-Related Changes of the Pattern of Non-Histone Chromatin Proteins from Rat and Mouse Liver Chromatin

Gerontology ◽  
1979 ◽  
Vol 25 (4) ◽  
pp. 219-227 ◽  
Author(s):  
Zh.A. Medvedev ◽  
M.N. Medvedeva ◽  
L. Robson
Keyword(s):  
Mouse Liver ◽  
Age Related ◽  
Liver Chromatin ◽  
Chromatin Proteins ◽  
Age Related Changes

scholarly journals STAT5 regulation of sex-dependent hepatic CpG methylation at distal regulatory elements mapping to sex-biased genes

2020 ◽  
Author(s):  
Pengying Hao ◽  
David J. Waxman
Keyword(s):  
Gene Expression ◽  
Sex Differences ◽  
Mouse Liver ◽  
Regulatory Elements ◽  
Cpg Methylation ◽  
Sex Bias ◽  
Liver Chromatin ◽  
Differential Gene ◽  
Genomic Regions ◽  
Distal Regulatory Elements

Growth hormone-activated STAT5b is an essential regulator of sex-differential gene expression in mouse liver, however, its impact on hepatic gene expression and epigenetic responses is poorly understood. Here, we found a substantial, albeit incomplete loss of liver sex bias in hepatocyte-specific STAT5a/STAT5b (collectively, STAT5)-deficient mouse liver. In male liver, many male-biased genes were down regulated in direct association with the loss of STAT5 binding; many female-biased genes, which show low STAT5 binding, were de-repressed, indicating an indirect mechanism for repression by STAT5. Extensive changes in CpG-methylation were seen in STAT5-deficient liver, where sex differences were abolished at 88% of ∼1,500 sex-differentially methylated regions, largely due to increased DNA methylation upon STAT5 loss. STAT5-dependent CpG-hypomethylation was rarely found at proximal promoters of STAT5-dependent genes. Rather, STAT5 primarily regulated the methylation of distal enhancers, where STAT5 deficiency induced widespread hypermethylation at genomic regions enriched for accessible chromatin, enhancer histone marks (H3K4me1, H3K27ac), STAT5 binding, and DNA motifs for STAT5 and other transcription factors implicated in liver sex differences. Thus, the sex-dependent binding of STAT5 to liver chromatin is closely linked to the sex-dependent demethylation of distal regulatory elements linked to STAT5-dependent genes important for liver sex bias.

scholarly journals Improved Annotation of Untargeted Metabolomics Data Through Buffer Modifications That Shift Adduct Mass and Intensity

2020 ◽  
Author(s):  
Wenyun Lu ◽  
Xi Xing ◽  
Lin Wang ◽  
Li Chen ◽  
Sisi Zhang ◽  
...  
Keyword(s):  
Mouse Liver ◽  
Mass Difference ◽  
Biological Species ◽  
Adduct Formation ◽  
Kegg Database ◽  
Metabolomics Data ◽  
Mammalian Tissues ◽  
Intensity Changes ◽  
Full Scan ◽  
Characteristic Mass

<p></p><p>Annotation of untargeted high-resolution full-scan LC-MS metabolomics data remains challenging due to individual metabolites generating multiple LC-MS peaks arising from isotopes, adducts and fragments. Adduct annotation is a particular challenge, as the same mass difference between peaks can arise from adduct formation, fragmentation, or different biological species. To address this, here we describe a Buffer Modification Workflow (BMW), in which the same sample is run by LC-MS in both liquid chromatography solvent with <sup>14</sup>NH<sub>3</sub>-acetate buffer, and in solvent with the buffer modified with <sup>15</sup>NH<sub>3</sub>-formate. Buffer switching results in characteristic mass and signal intensity changes for adduct peaks, facilitating their annotation. This relatively simple and convenient chromatography modification annotated yeast metabolomics data with similar effectiveness to growing the yeast in isotope-labeled media. Application to mouse liver data annotated both known metabolite and known adduct peaks with 95% accuracy. Overall, it identified 26% of ~ 27,000 liver LC-MS features as putative metabolites, of which ~ 2600 showed HMDB or KEGG database formula match. This workflow is well-suited to biological samples that cannot be readily isotope labeled, including plants, mammalian tissues, and tumors. </p><br><p></p>

scholarly journals STAT5 regulation of sex-dependent hepatic CpG methylation at distal regulatory elements mapping to sex-biased genes

2020 ◽  
Author(s):  
Pengying Hao ◽  
David J. Waxman
Keyword(s):  
Gene Expression ◽  
Sex Differences ◽  
Mouse Liver ◽  
Regulatory Elements ◽  
Cpg Methylation ◽  
Sex Bias ◽  
Liver Chromatin ◽  
Differential Gene ◽  
Genomic Regions ◽  
Distal Regulatory Elements

AbstractGrowth hormone-activated STAT5b is an essential regulator of sex-differential gene expression in mouse liver, however, its impact on hepatic gene expression and epigenetic responses is poorly understood. Here, we found a substantial, albeit incomplete loss of liver sex bias in hepatocyte-specific STAT5a/STAT5b (collectively, STAT5)-deficient mouse liver. In male liver, many male-biased genes were down regulated in direct association with the loss of STAT5 binding; many female-biased genes, which show low STAT5 binding, were de-repressed, indicating an indirect mechanism for repression by STAT5. Extensive changes in CpG-methylation were seen in STAT5-deficient liver, where sex differences in DNA methylation were abolished at 88% of ~1,500 differentially-methylated regions, largely due to an increase in methylation at the hypomethylated sites. STAT5-dependent CpG-hypomethylation was rarely found at proximal promoters of STAT5-dependent genes. Rather, STAT5 primarily regulated the methylation of distal enhancers, where STAT5 deficiency induced widespread hypermethylation at genomic regions enriched for accessible chromatin, enhancer histone marks (H3K4me1, H3K27ac), STAT5 binding, and DNA motifs for STAT5 and other transcription factors implicated in liver sex differences. In conclusion, the sex-dependent binding of STAT5 to liver chromatin is closely linked to sex-dependent demethylation of distal regulatory elements mapping to STAT5-dependent genes important for liver sex bias.

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