On the fiftieth anniversary of the Schaechter, Maaløe, Kjeldgaard experiments: implications for cell-cycle and cell-growth control

BioEssays ◽  
2008 ◽  
Vol 30 (10) ◽  
pp. 1019-1024 ◽  
Author(s):  
Stephen Cooper
Keyword(s):  
Cell Cycle ◽  
Cell Growth ◽  
Growth Control ◽  
Fiftieth Anniversary ◽  
Cell Growth Control

scholarly journals Diversification of retinoblastoma protein function associated with cis and trans adaptations

2018 ◽  
Author(s):  
Rima Mouawad ◽  
Jaideep Prasad ◽  
Dominic Thorley ◽  
Pamela Himadewi ◽  
Dhruva Kadiyala ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Growth ◽  
Target Genes ◽  
Growth Control ◽  
Retinoblastoma Protein ◽  
Egg Laying ◽  
Female Reproductive Tract ◽  
Abnormal Development ◽  
Cell Growth Control ◽  
Null Mutants

AbstractRetinoblastoma proteins are eukaryotic transcriptional co-repressors that play central roles in cell cycle control, among other functions. Although most metazoan genomes encode a single retinoblastoma protein, gene duplications have occurred at least twice: in the vertebrate lineage, leading to three genes encoding Rb, p107, and p130, while separately in the Drosophila lineage an ancestral Rbf1 gene and a derived Rbf2 gene. Structurally, Rbf1 resembles p107 and p130 most closely, and mutation of the gene is lethal, while Rbf2 is more divergent, and is not essential for development. Rbf1 has been demonstrated to be a potent repressor of canonical cell-cycle promoters, unlike Rbf2. The retention of Rbf2 over 60 million years in the entire Drosophila lineage points to essential functions, however. We show here that Rbf2 regulates a broad set of cell growth control related genes, and can antagonize Rbf1 on specific sets of promoters. Rbf2 null mutants exhibit abnormal development of the female reproductive tract, with reduced egg laying, while heterozygous null mutants exhibit an increased rate of egg deposition, suggesting that the normal function of this protein is critical for optimal control of fertility. The structural alterations found in conserved regions of the Rbf2 gene suggest that this gene was sub- or neofunctionalized to develop specific regulatory specificity and activity. We define cis regulatory features of Rbf2 target genes that allow preferential repression by this protein, indicating that it is not merely a weaker version of the ancestral protein. The specialization of retinoblastoma function in Drosophila may reflect a parallel evolution found in vertebrates, and raises the possibility that cell growth control is equally important to cell cycle function for this conserved family of transcriptional corepressors.

scholarly journals ei24, a p53 Response Gene Involved in Growth Suppression and Apoptosis

2000 ◽  
Vol 20 (1) ◽  
pp. 233-241 ◽  
Author(s):  
Zhengming Gu ◽  
Cathy Flemington ◽  
Thomas Chittenden ◽  
Gerard P. Zambetti
Keyword(s):  
Cell Cycle ◽  
Cell Growth ◽  
Tumor Suppressor ◽  
Cell Cycle Arrest ◽  
Apoptotic Cell ◽  
Functional Characterization ◽  
Growth Control ◽  
P53 Tumor Suppressor ◽  
Cycle Arrest ◽  
P53 Response

ABSTRACT DNA damage and/or hyperproliferative signals activate the wild-type p53 tumor suppressor protein, which induces a G1 cell cycle arrest or apoptosis. Although the mechanism of p53-mediated cell cycle arrest is fairly well defined, the p53-dependent pathway regulating apoptosis is poorly understood. Here we report the functional characterization of murine ei24 (also known asPIG8), a gene directly regulated by p53, whose overexpression negatively controls cell growth and induces apoptotic cell death. Ectopic ei24 expression markedly inhibits cell colony formation, induces the morphological features of apoptosis, and reduces the number of β-galactosidase-marked cells, which is efficiently blocked by coexpression of Bcl-XL. Theei24/PIG8 gene is localized on human chromosome 11q23, a region frequently altered in human cancers. These results suggest that ei24 may play an important role in negative cell growth control by functioning as an apoptotic effector of p53 tumor suppressor activities.

scholarly journals A new twist on cell growth control

Cell Cycle ◽  
2014 ◽  
Vol 13 (22) ◽  
pp. 3474-3475 ◽  
Author(s):  
Joseph F Cardiello ◽  
Jennifer F Kugel ◽  
James A Goodrich
Keyword(s):  
Cell Growth ◽  
Growth Control ◽  
Cell Growth Control

scholarly journals Long-range memory of growth and cycle progression correlates cell cycles in lineage trees

2018 ◽  
Author(s):  
Erika E Kuchen ◽  
Nils Becker ◽  
Nina Claudino ◽  
Thomas Höfer
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Cell Growth ◽  
Mammalian Cell ◽  
Latent Variable ◽  
Cycle Length ◽  
Growth Control ◽  
Minimum Size ◽  
Cell Cycles ◽  
Lineage Trees

Mammalian cell proliferation is controlled by mitogens. However, how proliferation is coordinated with cell growth is poorly understood. Here we show that statistical properties of cell lineage trees – the cell-cycle length correlations within and across generations – reveal how cell growth controls proliferation. Analyzing extended lineage trees with latent-variable models, we find that two antagonistic heritable variables account for the observed cycle-length correlations. Using molecular perturbations of mTOR and MYC we identify these variables as cell size and regulatory license to divide, which are coupled through a minimum-size checkpoint. The checkpoint is relevant only for fast cell cycles, explaining why growth control of mammalian cell proliferation has remained elusive. Thus, correlated fluctuations of the cell cycle encode its regulation.

Lysozyme-dependent Proliferation Switch: Hematopoietic and Hybridoma Cell Growth Control with the Use of Antibody/GP130 Chimera

2002 ◽  
pp. 337-341
Author(s):  
Masahiro Kawahara ◽  
Akito Natsume ◽  
Satoshi Terada ◽  
Koichi Kato ◽  
Kouhei Tsumoto ◽  
...  
Keyword(s):  
Cell Growth ◽  
Growth Control ◽  
Cell Growth Control
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