scholarly journals Notch Signaling and Developmental Cell-Cycle Arrest in Drosophila Polar Follicle Cells

2009 ◽  
Vol 20 (24) ◽  
pp. 5064-5073 ◽  
Author(s):  
Li-Fang Shyu ◽  
Jianjun Sun ◽  
Hui-Min Chung ◽  
Yi-Chun Huang ◽  
Wu-Min Deng
Keyword(s):  
Cell Cycle ◽  
Notch Signaling ◽  
Cell Cycle Arrest ◽  
Developmental Regulation ◽  
Cell Types ◽  
Follicle Cells ◽  
Cycle Arrest ◽  
G2 Phase ◽  
G2 Cell Cycle Arrest ◽  
Regulation Of Cell Cycle

Temporal and spatial regulation of cell division is critical for proper development of multicellular organisms. An important aspect of this regulation is cell-cycle arrest, which in many cell types is coupled with differentiated status. Here we report that the polar cells—a group of follicle cells differentiated early during Drosophila oogenesis—are arrested at G2 phase and can serve as a model cell type for investigation of developmental regulation of cell-cycle arrest. On examining the effects of String, a mitosis-promoting phosphatase Cdc25 homolog, and Notch signaling in polar cells, we found that misexpression of String can trigger mitosis in existing polar cells to induce extra polar cells. Normally, differentiation of the polar cells requires Notch signaling. We found that the Notch-induced extra polar cells arise through recruitment of the neighboring cells rather than promotion of proliferation, and they are also arrested at G2 phase. Notch signaling is probably involved in down-regulating String in polar cells, thus inducing the G2 cell-cycle arrest.

scholarly journals G1 versus G2 cell cycle arrest after adriamycin-induced damage in mouse Swiss3T3 cells

FEBS Letters ◽  
1999 ◽  
Vol 461 (3) ◽  
pp. 299-305 ◽  
Author(s):  
Wai Yi Siu ◽  
Cain H Yam ◽  
Randy Y.C Poon
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Cycle Arrest ◽  
G2 Cell Cycle Arrest

scholarly journals Muscle Stem Cells Undergo Extensive Clonal Drift during Tissue Growth via Meox1-Mediated Induction of G2 Cell-Cycle Arrest

2017 ◽  
Vol 21 (1) ◽  
pp. 107-119.e6 ◽  
Author(s):  
Phong Dang Nguyen ◽  
David Baruch Gurevich ◽  
Carmen Sonntag ◽  
Lucy Hersey ◽  
Sara Alaei ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Stem Cells ◽  
Cell Cycle Arrest ◽  
Tissue Growth ◽  
Muscle Stem Cells ◽  
Cycle Arrest ◽  
G2 Cell Cycle Arrest

scholarly journals Critical role of PP2A-B56 family protein degradation in HIV-1 Vif mediated G2 cell cycle arrest

2020 ◽  
Vol 527 (1) ◽  
pp. 257-263
Author(s):  
Kayoko Nagata ◽  
Keisuke Shindo ◽  
Yusuke Matsui ◽  
Kotaro Shirakawa ◽  
Akifumi Takaori-Kondo
Keyword(s):  
Cell Cycle ◽  
Protein Degradation ◽  
Cell Cycle Arrest ◽  
Critical Role ◽  
Cycle Arrest ◽  
Family Protein ◽  
G2 Cell Cycle Arrest ◽  
Hiv 1

scholarly journals Weighted Correlation Network Analysis Reveals CDK2 as a Regulator of a Ubiquitous Environmental Toxin-Induced Cell-Cycle Arrest

Cells ◽  
2020 ◽  
Vol 9 (1) ◽  
pp. 143
Author(s):  
Virginie Dubourg ◽  
Alexander Nolze ◽  
Michael Kopf ◽  
Michael Gekle ◽  
Gerald Schwerdt
Keyword(s):  
Cell Cycle ◽  
Network Analysis ◽  
Cell Cycle Arrest ◽  
Regulation Of Gene Expression ◽  
Correlation Network ◽  
Food Contaminants ◽  
Proximal Tubule Cells ◽  
Cycle Arrest ◽  
G2 Cell Cycle Arrest ◽  
Weighted Correlation

Environmental food contaminants constitute a threat to human health. For instance, the globally spread mycotoxin Ochratoxin A (OTA) contributes to chronic kidney damage by affecting proximal tubule cells via unknown mechanisms. We applied a top-down approach to identify relevant toxicological mechanisms of OTA using RNA-sequencing followed by in-depth bioinformatics analysis and experimental validation. Differential expression analyses revealed that OTA led to the regulation of gene expression in kidney human cell lines, including for genes enriched in cell cycle-related pathways, and OTA-induced gap 1 and 2 (G1 and G2) cell-cycle arrests were observed. Weighted correlation network analysis highlighted cyclin dependent kinase 2 (CDK2) as a putative key regulator of this effect. CDK2 was downregulated by OTA exposure, and its overexpression partially blocked the OTA-induced G1 but not G2 cell-cycle arrest. We, therefore, propose CDK2 as one of the key regulators of the G1 cell-cycle arrest induced by low nanomolar concentrations of OTA.

scholarly journals Hypoxia-Inducible Factor 1α Is Essential for Cell Cycle Arrest during Hypoxia

2003 ◽  
Vol 23 (1) ◽  
pp. 359-369 ◽  
Author(s):  
Nobuhito Goda ◽  
Heather E. Ryan ◽  
Bahram Khadivi ◽  
Wayne McNulty ◽  
Robert C. Rickert ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Transcription Factor ◽  
Cell Cycle Arrest ◽  
Cellular Response ◽  
Hypoxia Inducible Factor ◽  
Growth Arrest ◽  
Cell Types ◽  
Low Oxygen ◽  
Double Knockout ◽  
Cycle Arrest

ABSTRACT A classical cellular response to hypoxia is a cessation of growth. Hypoxia-induced growth arrest differs in different cell types but is likely an essential aspect of the response to wounding and injury. An important component of the hypoxic response is the activation of the hypoxia-inducible factor 1 (HIF-1) transcription factor. Although this transcription factor is essential for adaptation to low oxygen levels, the mechanisms through which it influences cell cycle arrest, including the degree to which it cooperates with the tumor suppressor protein p53, remain poorly understood. To determine broadly relevant aspects of HIF-1 function in primary cell growth arrest, we examined two different primary differentiated cell types which contained a deletable allele of the oxygen-sensitive component of HIF-1, the HIF-1α gene product. The two cell types were murine embryonic fibroblasts and splenic B lymphocytes; to determine how the function of HIF-1α influenced p53, we also created double-knockout (HIF-1α null, p53 null) strains and cells. In both cell types, loss of HIF-1α abolished hypoxia-induced growth arrest and did this in a p53-independent fashion. Surprisingly, in all cases, cells lacking both p53 and HIF-1α genes have completely lost the ability to alter the cell cycle in response to hypoxia. In addition, we have found that the loss of HIF-1α causes an increased progression into S phase during hypoxia, rather than a growth arrest. We show that hypoxia causes a HIF-1α-dependent increase in the expression of the cyclin-dependent kinase inhibitors p21 and p27; we also find that hypophosphorylation of retinoblastoma protein in hypoxia is HIF-1α dependent. These data demonstrate that the transcription factor HIF-1 is a major regulator of cell cycle arrest in primary cells during hypoxia.

scholarly journals Differential activation of target cellular promoters by p53 mutants with impaired apoptotic function.

1996 ◽  
Vol 16 (9) ◽  
pp. 4952-4960 ◽  
Author(s):  
R L Ludwig ◽  
S Bates ◽  
K H Vousden
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Dna Sequences ◽  
Transcriptional Activation ◽  
Cellular Response ◽  
Kinase Inhibitor ◽  
Cell Types ◽  
Cyclin Dependent Kinase Inhibitor ◽  
Cycle Arrest ◽  
P53 Tumor Suppressor Protein

The p53 tumor suppressor protein is a sequence-specific transcriptional activator, a function which contributes to cell cycle arrest and apoptosis induced by p53 in appropriate cell types. Analysis of a series of p53 point mutants has revealed the potential for selective loss of the ability to transactivate some, but not all, cellular p53-responsive promoters. p53 175P and p53 181L are tumor-derived p53 point mutants which were previously characterized as transcriptionally active. Both mutants retained the ability to activate expression of the cyclin-dependent kinase inhibitor p2lcip1/waf1, and this activity correlated with the ability to induce a G1 cell cycle arrest. However, an extension of this survey to include other p53 targets showed that p53 175P was defective in the activation of p53-responsive sequences derived from the bax promoter and the insulin-like growth factor-binding protein 3 gene (IGF-BP3) promoter, while p53 181L showed loss of the ability to activate a promoter containing IGF-BP3 box B sequences. Failure to activate transcription was also reflected in the reduced ability of the mutants to bind the p53-responsive DNA sequences present in these promoters. These specific defects in transcriptional activation correlated with the impaired apoptotic function displayed by these mutants, and the results suggest that activation of cell cycle arrest genes by p53 can be separated from activation of genes with a role in mediating the p53 apoptotic response. The cellular response to p53 activation may therefore depend, at least in part, on which group of p53-responsive genes become transcriptionally activated.

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