scholarly journals Differentiation-associated microRNAs antagonize the Rb–E2F pathway to restrict proliferation

2012 ◽  
Vol 199 (1) ◽  
pp. 77-95 ◽  
Author(s):  
Matteo J. Marzi ◽  
Eleonora M. R. Puggioni ◽  
Valentina Dall'Olio ◽  
Gabriele Bucci ◽  
Loris Bernard ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Posttranscriptional Regulation ◽  
Cell Cycle Control ◽  
Terminal Differentiation ◽  
Model System ◽  
Cell Cycle Reentry ◽  
Dependent Cell ◽  
Specific Factors ◽  
Proliferative Advantage

The cancer-associated loss of microRNA (miRNA) expression leads to a proliferative advantage and aggressive behavior through largely unknown mechanisms. Here, we exploit a model system that recapitulates physiological terminal differentiation and its reversal upon oncogene expression to analyze coordinated mRNA/miRNA responses. The cell cycle reentry of myotubes, forced by the E1A oncogene, was associated with a pattern of mRNA/miRNA modulation that was largely reciprocal to that induced during the differentiation of myoblasts into myotubes. The E1A-induced mRNA response was preponderantly Retinoblastoma protein (Rb)-dependent. Conversely, the miRNA response was mostly Rb-independent and exerted through tissue-specific factors and Myc. A subset of these miRNAs (miR-1, miR-34, miR-22, miR-365, miR-29, miR-145, and Let-7) was shown to coordinately target Rb-dependent cell cycle and DNA replication mRNAs. Thus, a dual level of regulation—transcriptional regulation via Rb–E2F and posttranscriptional regulation via miRNAs—confers robustness to cell cycle control and provides a molecular basis to understand the role of miRNA subversion in cancer.

Role of transcriptional and posttranscriptional regulation in expression of histone genes in Saccharomyces cerevisiae

1987 ◽  
Vol 7 (2) ◽  
pp. 614-621
Author(s):  
D E Lycan ◽  
M A Osley ◽  
L M Hereford
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Dna Replication ◽  
Posttranscriptional Regulation ◽  
Cell Cycle Control ◽  
Dimensional Structure ◽  
Histone Genes ◽  
Transcriptional Regulatory Mechanisms ◽  
Rna Levels

We analyzed the role of posttranscriptional mechanisms in the regulation of histone gene expression in Saccharomyces cerevisiae. The rapid drop in histone RNA levels associated with the inhibition of ongoing DNA replication was postulated to be due to posttranscriptional degradation of histone transcripts. However, in analyzing the sequences required for this response, we showed that the coupling of histone RNA levels to DNA replication was due mostly, if not entirely, to transcriptional regulatory mechanisms. Furthermore, deletions which removed the negative, cell cycle control sequences from the histone promoter also uncoupled histone transcription from DNA replication. We propose that the arrest of DNA synthesis prematurely activates the regulatory pathway used in the normal cell cycle to repress transcription. Although posttranscriptional regulation did not appear to play a significant role in coupling histone RNA levels to DNA replication, it did affect the levels of histone RNA in the cell cycle. Posttranscriptional regulation could apparently restore much of the periodicity of histone RNA accumulation in cells which constitutively transcribed the histone genes. Unlike transcriptional regulation, periodic posttranscriptional regulation appears to operate on a clock which is independent of events in the mitotic DNA cycle. Posttranscriptional recognition of histone RNA must require either sequences in the 3' end of the RNA or an intact three-dimensional structure since H2A- and H2B-lacZ fusion transcripts, containing only 5' histone sequences, were insensitive to posttranscriptional controls.

scholarly journals Role of transcriptional and posttranscriptional regulation in expression of histone genes in Saccharomyces cerevisiae.

1987 ◽  
Vol 7 (2) ◽  
pp. 614-621 ◽  
Author(s):  
D E Lycan ◽  
M A Osley ◽  
L M Hereford
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Dna Replication ◽  
Posttranscriptional Regulation ◽  
Cell Cycle Control ◽  
Dimensional Structure ◽  
Histone Genes ◽  
Transcriptional Regulatory Mechanisms ◽  
Rna Levels

We analyzed the role of posttranscriptional mechanisms in the regulation of histone gene expression in Saccharomyces cerevisiae. The rapid drop in histone RNA levels associated with the inhibition of ongoing DNA replication was postulated to be due to posttranscriptional degradation of histone transcripts. However, in analyzing the sequences required for this response, we showed that the coupling of histone RNA levels to DNA replication was due mostly, if not entirely, to transcriptional regulatory mechanisms. Furthermore, deletions which removed the negative, cell cycle control sequences from the histone promoter also uncoupled histone transcription from DNA replication. We propose that the arrest of DNA synthesis prematurely activates the regulatory pathway used in the normal cell cycle to repress transcription. Although posttranscriptional regulation did not appear to play a significant role in coupling histone RNA levels to DNA replication, it did affect the levels of histone RNA in the cell cycle. Posttranscriptional regulation could apparently restore much of the periodicity of histone RNA accumulation in cells which constitutively transcribed the histone genes. Unlike transcriptional regulation, periodic posttranscriptional regulation appears to operate on a clock which is independent of events in the mitotic DNA cycle. Posttranscriptional recognition of histone RNA must require either sequences in the 3' end of the RNA or an intact three-dimensional structure since H2A- and H2B-lacZ fusion transcripts, containing only 5' histone sequences, were insensitive to posttranscriptional controls.

The Arabidopsis leaf as a model system for investigating the role of cell cycle regulation in organ growth

2005 ◽  
Vol 119 (1) ◽  
pp. 43-50 ◽  
Author(s):  
Gerrit T. S. Beemster ◽  
Steven Vercruysse ◽  
Lieven De Veylder ◽  
Martin Kuiper ◽  
Dirk Inzé
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Regulation ◽  
Model System ◽  
Organ Growth ◽  
Cycle Regulation

The role of MCM proteins in the cell cycle control of genome duplication

BioEssays ◽  
1996 ◽  
Vol 18 (3) ◽  
pp. 183-190 ◽  
Author(s):  
Stephen E. Kearsey ◽  
Domenico Maiorano ◽  
Eddie C. Holmes ◽  
Ivan T. Todorov
Keyword(s):  
Cell Cycle ◽  
Genome Duplication ◽  
Cell Cycle Control ◽  
Mcm Proteins

scholarly journals Wip1 Regulates the Generation of New Neural Cells in the Adult Olfactory Bulb through p53-Dependent Cell Cycle Control

Stem Cells ◽  
2009 ◽  
Vol 27 (6) ◽  
pp. 1433-1442 ◽  
Author(s):  
Yun-Hua Zhu ◽  
Cheng-Wu Zhang ◽  
Li Lu ◽  
Oleg N. Demidov ◽  
Li Sun ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Olfactory Bulb ◽  
Cell Cycle Control ◽  
Neural Cells ◽  
Dependent Cell

Cell cycle- and terminal differentiation-associated regulation of the mouse mRNA encoding a conserved mitotic protein kinase

1993 ◽  
Vol 13 (12) ◽  
pp. 7793-7801
Author(s):  
R J Lake ◽  
W R Jelinek
Keyword(s):  
Cell Cycle ◽  
Protein Kinase ◽  
Posttranscriptional Regulation ◽  
Terminal Differentiation ◽  
The Body ◽  
Erythroleukemia Cells ◽  
M Phase ◽  
Erythroleukemia Cell ◽  
Low Levels ◽  
Murine Erythroleukemia

We determined the nucleotide sequence of a mouse and a human cDNA, which we designate STPK13, that encodes an apparent protein kinase related to that encoded by the Drosophila melanogaster polo gene and the Saccharomyces cerevisiae CDC5 gene. The polo and CDC5 gene products are required for normal mitosis. The STPK13 mRNA is regulated during terminal erythrodifferentiation and during the cell cycle. Within the precommitment period of murine erythroleukemia cell terminal differentiation, most of the poly(A) tail is lost from the STPK13 mRNA, but the body of the mRNA remains unchanged in abundance; this poly(A) loss does not occur in mutant erythroleukemia cells that fail to commit to terminal differentiation. During the cell cycle, the abundance of the body of the STPK13 mRNA fluctuates. The mRNA is present in growing but not in nongrowing cells. It reaches a maximum abundance during G2/M phase, is absent or present at only low levels during G1 phase, and begins to reaccumulate at approximately the middle of S phase. The cell cycle-associated accumulation and loss of the STPK13 mRNA could cause a similar fluctuation in abundance of its encoded protein kinase, thereby providing a maximum amount during M phase, when the kinase is thought to function, and little or none at other times of the cell cycle. Posttranscriptional regulation must be responsible for the cell cycle-associated fluctuations because transcription rates are relatively constant during different times of the cell cycle when there are large differences in mRNA abundance.

scholarly journals Role of D-GADD45 in JNK-Dependent Apoptosis and Regeneration in Drosophila

Genes ◽  
2019 ◽  
Vol 10 (5) ◽  
pp. 378 ◽  
Author(s):  
Carlos Camilleri-Robles ◽  
Florenci Serras ◽  
Montserrat Corominas
Keyword(s):  
Cell Cycle ◽  
Cell Death ◽  
Cell Cycle Control ◽  
Imaginal Discs ◽  
Cellular Functions ◽  
Correct Function ◽  
Response To Stress ◽  
Wing Imaginal Discs ◽  
Harmful Effects

The GADD45 proteins are induced in response to stress and have been implicated in the regulation of several cellular functions, including DNA repair, cell cycle control, senescence, and apoptosis. In this study, we investigate the role of D-GADD45 during Drosophila development and regeneration of the wing imaginal discs. We find that higher expression of D-GADD45 results in JNK-dependent apoptosis, while its temporary expression does not have harmful effects. Moreover, D-GADD45 is required for proper regeneration of wing imaginal discs. Our findings demonstrate that a tight regulation of D-GADD45 levels is required for its correct function both, in development and during the stress response after cell death.

Abnormalities in Cell Cycle Control in Cancer and Their Clinical Implications

1998 ◽  
Vol 84 (4) ◽  
pp. 421-433 ◽  
Author(s):  
Alessandro Sgambato ◽  
Giovanna Flamini ◽  
Achille Cittadini ◽  
I. Bernard Weinstein
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Transformation ◽  
Cell Cycle Control ◽  
Genomic Stability ◽  
Clinical Implications ◽  
Mammalian Cell Cycle ◽  
Carcinogenic Process ◽  
Review Current

Recent studies indicate that the functions of several genes that control the cell cycle are altered during the carcinogenic process and that these changes perturb both cell proliferation and genomic stability, thus promoting cell transformation and enhancing the process of tumor progression. The purpose of this paper is to review current information on the role of cyclins and related genes in the control of the mammalian cell cycle, the types of abnormalities in these genes found in human tumors and the possible clinical implications of these findings.

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