scholarly journals DNase I and micrococcal nuclease analysis of the tomato proteinase inhibitor I gene in chromatin.

1993 ◽  
Vol 268 (1) ◽  
pp. 430-435
Author(s):  
A. Conconi ◽  
C.A. Ryan
Keyword(s):  
Proteinase Inhibitor ◽  
Dnase I ◽  
Micrococcal Nuclease ◽  
I Gene

Butyrate-induced changes in nuclease sensitivity of chromatin cannot be correlated with transcriptional activation

1987 ◽  
Vol 7 (11) ◽  
pp. 3863-3870
Author(s):  
B W Birren ◽  
S J Taplitz ◽  
H R Herschman
Keyword(s):  
Transcriptional Activation ◽  
Hepatoma Cell ◽  
Dnase I ◽  
Micrococcal Nuclease ◽  
Hepatoma Cell Line ◽  
Butyrate Treatment ◽  
Dnase I Sensitivity ◽  
Induced Changes ◽  
I Gene ◽  
Nuclease Sensitivity

We examined in the H4IIE rat hepatoma cell line the relationship between butyrate-induced changes in the nuclease sensitivity of chromatin and changes in transcriptional activity of specific genes. The butyrate-inducible metallothionein I (MT-I) gene underwent a dramatic increase in DNase I sensitivity after 3 h of butyrate treatment. However, genes not transcribed in H4IIE cells underwent the same changes in DNase I sensitivity. Thus, butyrate-induced increases in DNase I sensitivity are not sufficient for the transcriptional activation of a gene. Butyrate treatment has also been reported to alter the sensitivity of sequences to micrococcal nuclease (MNase) in a manner reflecting their tissue-specific expression. Butyrate exposure caused increased digestion of the MT-I gene by MNase. However, butyrate-induced MNase sensitivity also occurred for genes which are neither transcribed in untreated cells nor butyrate inducible. Moreover, cadmium, a potent transcriptional activator of the MT-I gene, does not alter the sensitivity of the MT-I gene to MNase. Thus, the butyrate-induced alterations in MNase sensitivity are neither sufficient for, necessary for, nor indicative of transcriptional activation.

scholarly journals Butyrate-induced changes in nuclease sensitivity of chromatin cannot be correlated with transcriptional activation.

1987 ◽  
Vol 7 (11) ◽  
pp. 3863-3870 ◽  
Author(s):  
B W Birren ◽  
S J Taplitz ◽  
H R Herschman
Keyword(s):  
Transcriptional Activation ◽  
Hepatoma Cell ◽  
Dnase I ◽  
Micrococcal Nuclease ◽  
Hepatoma Cell Line ◽  
Butyrate Treatment ◽  
Dnase I Sensitivity ◽  
Induced Changes ◽  
I Gene ◽  
Nuclease Sensitivity

We examined in the H4IIE rat hepatoma cell line the relationship between butyrate-induced changes in the nuclease sensitivity of chromatin and changes in transcriptional activity of specific genes. The butyrate-inducible metallothionein I (MT-I) gene underwent a dramatic increase in DNase I sensitivity after 3 h of butyrate treatment. However, genes not transcribed in H4IIE cells underwent the same changes in DNase I sensitivity. Thus, butyrate-induced increases in DNase I sensitivity are not sufficient for the transcriptional activation of a gene. Butyrate treatment has also been reported to alter the sensitivity of sequences to micrococcal nuclease (MNase) in a manner reflecting their tissue-specific expression. Butyrate exposure caused increased digestion of the MT-I gene by MNase. However, butyrate-induced MNase sensitivity also occurred for genes which are neither transcribed in untreated cells nor butyrate inducible. Moreover, cadmium, a potent transcriptional activator of the MT-I gene, does not alter the sensitivity of the MT-I gene to MNase. Thus, the butyrate-induced alterations in MNase sensitivity are neither sufficient for, necessary for, nor indicative of transcriptional activation.

scholarly journals Maintenance of Open Chromatin and Selective Genomic Occupancy at the Cell Cycle-Regulated Histone H4 Promoter during Differentiation of HL-60 Promyelocytic Leukemia Cells

2003 ◽  
Vol 23 (4) ◽  
pp. 1460-1469 ◽  
Author(s):  
Hayk Hovhannisyan ◽  
Brian Cho ◽  
Partha Mitra ◽  
Martin Montecino ◽  
Gary S. Stein ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Kinase Inhibitor ◽  
Restriction Enzymes ◽  
Dnase I ◽  
Promyelocytic Leukemia ◽  
Micrococcal Nuclease ◽  
Leukemia Cells ◽  
N Gene ◽  
Open Chromatin ◽  
Histone H4

ABSTRACT During the shutdown of proliferation and onset of differentiation of HL-60 promyelocytic leukemia cells, expression of the cell cycle-dependent histone genes is downregulated at the level of transcription. To address the mechanism by which this regulation occurs, we examined the chromatin structure of the histone H4/n (FO108, H4FN) gene locus. Micrococcal nuclease, DNase I, and restriction enzymes show similar cleavage sites and levels of sensitivity at the H4/n locus in both proliferating and differentiated HL-60 cells. In contrast, differentiation-related activation of the cyclin-dependent kinase inhibitor p21cip1/WAF1 gene is accompanied by increased nuclease hypersensitivity. Chromatin immunoprecipitation assays of the H4/n gene reveal that acetylated histones H3 and H4 are maintained at the same levels in proliferating and postproliferative cells. Thus, the chromatin of the H4/n locus remains in an open state even after transcription ceases. Using ligation-mediated PCR to visualize genomic DNase I footprints at single-nucleotide resolution, we find that protein occupancy at the site II cell cycle element is selectively diminished in differentiated cells while the site I element remains occupied. Decreased occupancy of site II is reflected by loss of the site II binding protein HiNF-P. We conclude that H4 gene transcription during differentiation is downregulated by modulating protein interaction at the site II cell cycle element and that retention of an open chromatin conformation may be associated with site I occupancy.

Major histocompatibility complex class I genes in murine fibrosarcoma IC9 are down regulated at the level of the chromatin structure

1989 ◽  
Vol 9 (7) ◽  
pp. 3136-3142
Author(s):  
U Maschek ◽  
W Pülm ◽  
S Segal ◽  
G J Hämmerling
Keyword(s):  
Major Histocompatibility Complex ◽  
Major Histocompatibility Complex Class ◽  
Chromatin Structure ◽  
Dnase I ◽  
Class I ◽  
Micrococcal Nuclease ◽  
Complex Class ◽  
Major Histocompatibility ◽  
Histocompatibility Complex ◽  
Nuclear Extracts

The fibrosarcoma IC9 is deficient in the expression of the major histocompatibility complex class I genes Kb, Kk, and Dk and expresses only the Db molecule. Because class I deficiency may enable tumor cells to escape the immune response by cytotoxic T lymphocytes, we investigated why the class I genes are not expressed. Expression of the silent class I genes could not be induced, but all known DNA-binding factors specific for class I genes could be detected in nuclear extracts of IC9 cells. After cloning of the silent Kb gene from the IC9 cells and subsequent transfection of this cloned Kb gene into LTK- and IC9 cells, normal Kb antigens were expressed on the cell surface of both cell lines. Digestion of the chromatin of IC9 cells with micrococcal nuclease and DNase I showed a decreased nuclease sensitivity of the silent class I genes in comparison with active genes and the absence of DNase I hypersensitive sites in the promoter region of the silent Dk gene. These findings demonstrate that class I expression is turned off by a cis-acting regulatory mechanism at the level of the chromatin structure.

scholarly journals Formation of stable chromatin structures on the histone H4 gene during differentiation in Tetrahymena thermophila.

1986 ◽  
Vol 6 (8) ◽  
pp. 3014-3017 ◽  
Author(s):  
D S Pederson ◽  
K Shupe ◽  
G A Bannon ◽  
M A Gorovsky
Keyword(s):  
Chromatin Structure ◽  
Transcriptional Control ◽  
Tetrahymena Thermophila ◽  
Micrococcal Nuclease ◽  
Histone H4 ◽  
Hypersensitive Sites ◽  
Nuclear Differentiation ◽  
Histone Gene Transcription ◽  
The Relationship ◽  
I Gene

The relationship between chromatin structure and the transcriptional activity of the histone H4-I gene of Tetrahymena thermophila was explored. Indirect end-labeling studies demonstrated that major DNase I- and micrococcal nuclease-hypersensitive sites flank the active macronuclear genes but not the inactive micronuclear genes. Runon transcription experiments with isolated macronuclei indicated that histone gene transcription rates decreased when cells were starved. However, macronuclear nuclease-hypersensitive sites persisted upon starvation. Thus, one level of transcriptional control of the H4-I gene results in altered chromatin structure and is established during nuclear differentiation. The rate of transcription is also controlled, but not through hypersensitive site-associated structures.

scholarly journals Study of DNASE I gene polymorphisms in systemic lupus erythematosus susceptibility

2006 ◽  
Vol 66 (4) ◽  
pp. 560-561 ◽  
Author(s):  
A. Bodano ◽  
A. Gonzalez ◽  
E. Balada ◽  
J. Ordi ◽  
P. Carreira ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Gene Polymorphisms ◽  
Dnase I ◽  
Systemic Lupus ◽  
Systemic Lupus Erythematosus Susceptibility ◽  
I Gene

scholarly journals DNase I- and micrococcal nuclease-hypersensitive sites in the human apolipoprotein B gene are tissue specific.

1988 ◽  
Vol 8 (1) ◽  
pp. 71-80 ◽  
Author(s):  
B Levy-Wilson ◽  
C Fortier ◽  
B D Blackhart ◽  
B J McCarthy
Keyword(s):  
Hela Cells ◽  
Apolipoprotein B ◽  
Hepg2 Cells ◽  
Transcriptional Start Site ◽  
Dnase I ◽  
Micrococcal Nuclease ◽  
Apo B ◽  
Human Apolipoprotein ◽  
Hypersensitive Sites ◽  
High Degree

We have mapped the DNase I- and micrococcal nuclease-hypersensitive sites present in the 5' end of the human apolipoprotein B (apo-B) gene in nuclei from cells expressing or not expressing the gene. Four DNase I-hypersensitive sites were found in nuclei from liver-derived HepG2 cells and intestine-derived CaCo-2 cells, which express the apo-B gene, but not in HeLa cells, which do not. These sites are located near positions -120, -440, -700, and +760 base pairs relative to the transcriptional start site. Undifferentiated CaCo-2 cells exhibited another site, near position -540. Six micrococcal nuclease-hypersensitive sites were found in nuclei from HepG2 and CaCo-2 cells, but not in HeLa cells or free DNA. These sites are located near positions -120, -390, -530, -700, -850, and +210. HepG2 cells exhibited another site, near position +460. Comparison of the DNA sequence of the 5' flanking regions of the human and mouse apo-B genes revealed a high degree of evolutionary conservation of short stretches of sequences in the immediate vicinity of each of the DNase I- and most of the micrococcal nuclease-hypersensitive sites.

Sign in / Sign up

Export Citation Format

Share Document