Histone gene expression remains coupled to DNA synthesis during in vitro cellular senescence

1987 ◽  
Vol 172 (2) ◽  
pp. 397-403 ◽  
Author(s):  
Gerard Zambetti ◽  
Robert Dell'Orco ◽  
Gary Stein ◽  
Janet Stein
Keyword(s):  
Gene Expression ◽  
Dna Synthesis ◽  
Cellular Senescence ◽  
Histone Gene ◽  
Histone Gene Expression

scholarly journals Effect of adenovirus infection on expression of human histone genes.

1984 ◽  
Vol 4 (7) ◽  
pp. 1363-1371 ◽  
Author(s):  
S J Flint ◽  
M A Plumb ◽  
U C Yang ◽  
G S Stein ◽  
J L Stein
Keyword(s):  
Gene Expression ◽  
Dna Synthesis ◽  
Histone Gene ◽  
Adenovirus Infection ◽  
Histone Genes ◽  
Histone Mrna ◽  
Intact Cells ◽  
Mrna Species ◽  
Histone Gene Expression ◽  
Infected Cells

The influence of adenovirus type 2 infection of HeLa cells upon expression of human histone genes was examined as a function of the period of infection. Histone RNA synthesis was assayed after run-off transcription in nuclei isolated from mock-infected cells and after various periods of adenovirus infection. Histone protein synthesis was measured by [3H]leucine labeling of intact cells and fluorography of electrophoretically fractionated nuclear and cytoplasmic proteins. The cellular representation of RNA species complementary to more than 13 different human histone genes was determined by RNA blot analysis of total cellular, nuclear or cytoplasmic RNA by using a series of 32P-labeled cloned human histone genes as hybridization probes and also by analysis of 3H-labeled histone mRNA species synthesized in intact cells. By 18 h after infection, HeLa cell DNA synthesis and all parameters of histone gene expression, including transcription and the nuclear and cytoplasmic concentrations of core and H1 mRNA species, were reduced to less than 5 to 10% of the control values. By contrast, transcription and processing of other cellular mRNA sequences have been shown to continue throughout this period of infection. The early period of adenovirus infection was marked by an inhibition of transcription of histone genes that accompanied the reduction in rate of HeLa cell DNA synthesis. These results suggest that the adenovirus-induced inhibition of histone gene expression is mediated in part at the transcriptional level. However, the persistence of histone mRNA species at concentrations comparable to those of mock-infected control cells during the early phase of the infection, despite a reduction in histone gene transcription and histone protein synthesis, implies that histone gene expression is also regulated post-transcriptionally in adenovirus-infected cells. These results suggest that the tight coupling between histone mRNA concentrations and the rate of cellular DNA synthesis, observed when DNA replication is inhibited by a variety of drugs, is not maintained after adenovirus infection.

scholarly journals Role for a YY1-Binding Element in Replication-Dependent Mouse Histone Gene Expression

1998 ◽  
Vol 18 (12) ◽  
pp. 7106-7118 ◽  
Author(s):  
Katherine A. Eliassen ◽  
Amy Baldwin ◽  
Eric M. Sikorski ◽  
Myra M. Hurt
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Transcription Factor ◽  
Protein Interaction ◽  
Histone Gene ◽  
Cycle Phase ◽  
Histone Gene Expression ◽  
Dna Protein Interaction

ABSTRACT Expression of the highly conserved replication-dependent histone gene family increases dramatically as a cell enters the S phase of the eukaryotic cell cycle. Requirements for normal histone gene expression in vivo include an element, designated α, located within the protein-encoding sequence of nucleosomal histone genes. Mutation of 5 of 7 nucleotides of the mouse H3.2 α element to yield the sequence found in an H3.3 replication-independent variant abolishes the DNA-protein interaction in vitro and reduces expression fourfold in vivo. A yeast one-hybrid screen of a HeLa cell cDNA library identified the protein responsible for recognition of the histone H3.2 α sequence as the transcription factor Yin Yang 1 (YY1). YY1 is a ubiquitous and highly conserved transcription factor reported to be involved in both activation and repression of gene expression. Here we report that the in vitro histone α DNA-protein interaction depends on YY1 and that mutation of the nucleotides required for the in vitro histone α DNA-YY1 interaction alters the cell cycle phase-specific up-regulation of the mouse H3.2 gene in vivo. Because all mutations or deletions of the histone α sequence both abolish interactions in vitro and cause an in vivo decrease in histone gene expression, the recognition of the histone α element by YY1 is implicated in the correct temporal regulation of replication-dependent histone gene expression in vivo.

scholarly journals The Transcriptional Cofactor MCAF1/ATF7IP Is Involved in Histone Gene Expression and Cellular Senescence

PLoS ONE ◽  
2013 ◽  
Vol 8 (7) ◽  
pp. e68478 ◽  
Author(s):  
Nobuhiro Sasai ◽  
Noriko Saitoh ◽  
Hisato Saitoh ◽  
Mitsuyoshi Nakao
Keyword(s):  
Gene Expression ◽  
Cellular Senescence ◽  
Histone Gene ◽  
Histone Gene Expression

Histone gene switching in murine erythroleukemia cells is differentiation specific and occurs without loss of cell cycle regulation

1988 ◽  
Vol 8 (10) ◽  
pp. 4406-4415
Author(s):  
D T Brown ◽  
Y S Yang ◽  
D B Sittman
Keyword(s):  
Gene Expression ◽  
Dna Synthesis ◽  
Histone Gene ◽  
Mrna Levels ◽  
Hexamethylene Bisacetamide ◽  
Histone Gene Expression ◽  
Erythroleukemia Cells ◽  
Murine Erythroleukemia ◽  
Gene Switching ◽  
Cycle Regulation

We investigated the expression characteristics of the fully replication-dependent (FRD) and the partially replication-dependent (PRD) histone gene variants by measuring changes in steady-state mRNA levels during hexamethylene bisacetamide (HMBA)-induced differentiation of murine erythroleukemia (MEL) cells. Between 24 and 60 h after induction, there was a dramatic switch in histone gene expression, such that the ratio of PRD to FRD transcripts increased severalfold over that found in uninduced MEL cells. We demonstrated that this gene switching was not simply a partial or complete uncoupling of PRD gene expression from DNA synthesis. PRD and FRD transcript levels were regulated coordinately upon treatment of uninduced or induced MEL cells with inhibitors of DNA synthesis, protein synthesis, or both. Using several criteria, we were unable to detect any difference in PRD and FRD gene expression under any conditions except in cells undergoing differentiation. MEL cells were arrested at a precommitment stage of differentiation by induction with HMBA in the presence of dexamethasone (DEX). If DEX was subsequently removed, DNA synthesis resumed, the cells underwent commitment, and histone gene switching was observed. In contrast, if both DEX and HMBA were removed, DNA synthesis still resumed, but commitment did not occur and no gene switching was observed. These results imply that histone gene switching is intimately related to the differentiation process.

scholarly journals Distinct replication-independent and -dependent phases of histone gene expression during the Physarum cell cycle.

1987 ◽  
Vol 7 (5) ◽  
pp. 1933-1937 ◽  
Author(s):  
J J Carrino ◽  
V Kueng ◽  
R Braun ◽  
T G Laffler
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Dna Replication ◽  
Dna Synthesis ◽  
S Phase ◽  
Histone Gene ◽  
Histone Mrna ◽  
Histone Gene Expression ◽  
Tightly Coupled ◽  
G2 Phase

During the S phase of the cell cycle, histone gene expression and DNA replication are tightly coupled. In mitotically synchronous plasmodia of the myxomycete Physarum polycephalum, which has no G1 phase, histone mRNA synthesis begins in mid-G2 phase. Although histone gene transcription is activated in the absence of significant DNA synthesis, our data demonstrate that histone gene expression became tightly coupled to DNA replication once the S phase began. There was a transition from the replication-independent phase to the replication-dependent phase of histone gene expression. During the first phase, histone mRNA synthesis appears to be under direct cell cycle control; it was not coupled to DNA replication. This allowed a pool of histone mRNA to accumulate in late G2 phase, in anticipation of future demand. The second phase began at the end of mitosis, when the S phase began, and expression became homeostatically coupled to DNA replication. This homeostatic control required continuing protein synthesis, since cycloheximide uncoupled transcription from DNA synthesis. Nuclear run-on assays suggest that in P. polycephalum this coupling occurs at the level of transcription. While histone gene transcription appears to be directly switched on in mid-G2 phase and off at the end of the S phase by cell cycle regulators, only during the S phase was the level of transcription balanced with the rate of DNA synthesis.

scholarly journals Histone gene switching in murine erythroleukemia cells is differentiation specific and occurs without loss of cell cycle regulation.

1988 ◽  
Vol 8 (10) ◽  
pp. 4406-4415 ◽  
Author(s):  
D T Brown ◽  
Y S Yang ◽  
D B Sittman
Keyword(s):  
Gene Expression ◽  
Dna Synthesis ◽  
Histone Gene ◽  
Mrna Levels ◽  
Hexamethylene Bisacetamide ◽  
Histone Gene Expression ◽  
Erythroleukemia Cells ◽  
Murine Erythroleukemia ◽  
Gene Switching ◽  
Cycle Regulation

We investigated the expression characteristics of the fully replication-dependent (FRD) and the partially replication-dependent (PRD) histone gene variants by measuring changes in steady-state mRNA levels during hexamethylene bisacetamide (HMBA)-induced differentiation of murine erythroleukemia (MEL) cells. Between 24 and 60 h after induction, there was a dramatic switch in histone gene expression, such that the ratio of PRD to FRD transcripts increased severalfold over that found in uninduced MEL cells. We demonstrated that this gene switching was not simply a partial or complete uncoupling of PRD gene expression from DNA synthesis. PRD and FRD transcript levels were regulated coordinately upon treatment of uninduced or induced MEL cells with inhibitors of DNA synthesis, protein synthesis, or both. Using several criteria, we were unable to detect any difference in PRD and FRD gene expression under any conditions except in cells undergoing differentiation. MEL cells were arrested at a precommitment stage of differentiation by induction with HMBA in the presence of dexamethasone (DEX). If DEX was subsequently removed, DNA synthesis resumed, the cells underwent commitment, and histone gene switching was observed. In contrast, if both DEX and HMBA were removed, DNA synthesis still resumed, but commitment did not occur and no gene switching was observed. These results imply that histone gene switching is intimately related to the differentiation process.

Distinct replication-independent and -dependent phases of histone gene expression during the Physarum cell cycle

1987 ◽  
Vol 7 (5) ◽  
pp. 1933-1937
Author(s):  
J J Carrino ◽  
V Kueng ◽  
R Braun ◽  
T G Laffler
Keyword(s):  
Gene Expression ◽  
Cell Cycle ◽  
Dna Replication ◽  
Dna Synthesis ◽  
S Phase ◽  
Histone Gene ◽  
Histone Mrna ◽  
Histone Gene Expression ◽  
Tightly Coupled ◽  
G2 Phase

During the S phase of the cell cycle, histone gene expression and DNA replication are tightly coupled. In mitotically synchronous plasmodia of the myxomycete Physarum polycephalum, which has no G1 phase, histone mRNA synthesis begins in mid-G2 phase. Although histone gene transcription is activated in the absence of significant DNA synthesis, our data demonstrate that histone gene expression became tightly coupled to DNA replication once the S phase began. There was a transition from the replication-independent phase to the replication-dependent phase of histone gene expression. During the first phase, histone mRNA synthesis appears to be under direct cell cycle control; it was not coupled to DNA replication. This allowed a pool of histone mRNA to accumulate in late G2 phase, in anticipation of future demand. The second phase began at the end of mitosis, when the S phase began, and expression became homeostatically coupled to DNA replication. This homeostatic control required continuing protein synthesis, since cycloheximide uncoupled transcription from DNA synthesis. Nuclear run-on assays suggest that in P. polycephalum this coupling occurs at the level of transcription. While histone gene transcription appears to be directly switched on in mid-G2 phase and off at the end of the S phase by cell cycle regulators, only during the S phase was the level of transcription balanced with the rate of DNA synthesis.

scholarly journals Effect of adenovirus infection on expression of human histone genes

1984 ◽  
Vol 4 (7) ◽  
pp. 1363-1371
Author(s):  
S J Flint ◽  
M A Plumb ◽  
U C Yang ◽  
G S Stein ◽  
J L Stein
Keyword(s):  
Gene Expression ◽  
Dna Synthesis ◽  
Histone Gene ◽  
Adenovirus Infection ◽  
Histone Genes ◽  
Histone Mrna ◽  
Intact Cells ◽  
Mrna Species ◽  
Histone Gene Expression ◽  
Infected Cells

The influence of adenovirus type 2 infection of HeLa cells upon expression of human histone genes was examined as a function of the period of infection. Histone RNA synthesis was assayed after run-off transcription in nuclei isolated from mock-infected cells and after various periods of adenovirus infection. Histone protein synthesis was measured by [3H]leucine labeling of intact cells and fluorography of electrophoretically fractionated nuclear and cytoplasmic proteins. The cellular representation of RNA species complementary to more than 13 different human histone genes was determined by RNA blot analysis of total cellular, nuclear or cytoplasmic RNA by using a series of 32P-labeled cloned human histone genes as hybridization probes and also by analysis of 3H-labeled histone mRNA species synthesized in intact cells. By 18 h after infection, HeLa cell DNA synthesis and all parameters of histone gene expression, including transcription and the nuclear and cytoplasmic concentrations of core and H1 mRNA species, were reduced to less than 5 to 10% of the control values. By contrast, transcription and processing of other cellular mRNA sequences have been shown to continue throughout this period of infection. The early period of adenovirus infection was marked by an inhibition of transcription of histone genes that accompanied the reduction in rate of HeLa cell DNA synthesis. These results suggest that the adenovirus-induced inhibition of histone gene expression is mediated in part at the transcriptional level. However, the persistence of histone mRNA species at concentrations comparable to those of mock-infected control cells during the early phase of the infection, despite a reduction in histone gene transcription and histone protein synthesis, implies that histone gene expression is also regulated post-transcriptionally in adenovirus-infected cells. These results suggest that the tight coupling between histone mRNA concentrations and the rate of cellular DNA synthesis, observed when DNA replication is inhibited by a variety of drugs, is not maintained after adenovirus infection.

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