Neurotrophic control of the cell cycle during amphibian limb regeneration

Development ◽  
1978 ◽  
Vol 48 (1) ◽  
pp. 169-175
Author(s):  
M. Maden
Keyword(s):  
Cell Cycle ◽  
Dna Synthesis ◽  
Recent Work ◽  
Limb Regeneration ◽  
Trophic Factor ◽  
G1 Phase ◽  
Neurotrophic Control ◽  
G2 Phase ◽  
Number Of Cells

It is shown here that amputated and denervated limbs of larval axolotls dedifferentiate and a proportion of the cells released undergo DNA synthesis and mitosis. When the limb is denervated prior to amputation fewer cells go through the cell cycle, implying the existence of a pool of trophic factor in the limb. Recent work has demonstrated that denervated blastemal cells accumulate in the G1 phase of the cycle. These results strongly argue against the theory that the trophic factor controls the G2 phase. Rather, it is proposed that this factor regulates either the total number of cells cycling or the rate at which they cycle by varying the length of the G1 phase.

The Effect of 2-Phenyl Ethanol on the DNA Synthesis Cycle of Schizosaccharomyces Pombe

1970 ◽  
Vol 7 (2) ◽  
pp. 523-530
Author(s):  
C. J. BOSTOCK
Keyword(s):  
Cell Cycle ◽  
Dna Synthesis ◽  
Schizosaccharomyces Pombe ◽  
Normal Growth ◽  
S Phase ◽  
G1 Phase ◽  
Synchronous Cultures ◽  
Number Of Cells

The effect of different concentrations of 2-phenyl ethanol (PE) on growth and DNA synthesis of Schizosaccharomyces pombe is described. o.3% PE inhibits the entry of cells into S phase, but allows a doubling in the number of cells in the culture. The effect of o.2% PE on random and synchronous cultures of S. pombe shows that, in the continued presence of the inhibitor, the S phase is moved to a different point in the cell cycle. Cells continue to grow in the presence of o.2% PE with a G1 phase occupying a significant portion of the cell cycle. This differs from normal growth when the G1 phase is absent.

Post-transcriptional control of the onset of DNA synthesis by an insulin-like growth factor

1984 ◽  
Vol 4 (9) ◽  
pp. 1807-1814
Author(s):  
J Campisi ◽  
A B Pardee
Keyword(s):  
Cell Cycle ◽  
Growth Factors ◽  
Growth Factor ◽  
Dna Synthesis ◽  
Transcriptional Control ◽  
S Phase ◽  
G1 Phase ◽  
Insulin Like Growth Factor ◽  
Igf I ◽  
Translational Inhibition

The control of eucaryotic cell proliferation is governed largely by a series of regulatory events which occur in the G1 phase of the cell cycle. When stimulated to proliferate, quiescent (G0) 3T3 fibroblasts require transcription, rapid translation, and three growth factors for the growth state transition. We examined exponentially growing 3T3 cells to relate the requirements for G1 transit to those necessary for the transition from the G0 to the S phase. Cycling cells in the G1 phase required transcription, rapid translation, and a single growth factor (insulin-like growth factor [IGF] I) to initiate DNA synthesis. IGF I acted post-transcriptionally at a late G1 step. All cells in the G1 phase entered the S phase on schedule if either insulin (hyperphysiological concentration) or IGF I (subnanomolar concentration) was provided as the sole growth factor. In medium lacking all growth factors, only cells within 2 to 3 h of the S phase were able to initiate DNA synthesis. Similarly, cells within 2 to 3 h of the S phase were less dependent on transcription and translation for entry into the S phase. Cells responded very differently to inhibited translation than to growth factor deprivation. Cells in the early and mid-G1 phases did not progress toward the S phase during transcriptional or translational inhibition, and during translational inhibition they actually regressed from the S phase. In the absence of growth factors, however, these cells continued progressing toward the S phase, but still required IGF at a terminal step before initiating DNA synthesis. We conclude that a suboptimal condition causes cells to either progress or regress in the cell cycle rather than freezing them at their initial position. By using synchronized cultures, we also show that in contrast to earlier events, this final, IGF-dependent step did not require new transcription. This result is in contrast to findings that other growth factors induce new transcription. We examined the requirements for G1 transit by using a chemically transformed 3T3 cell line (BPA31 cells) which has lost some but not all ability to regulate its growth. Early- and mid-G1-phase BPA31 cells required transcription and translation to initiate DNA synthesis, although they did not regress from the S phase during translational inhibition. However, these cells did not need IGF for entry into the S phase.

Neurotrophic control of events in injured forelimbs of larval urodeles

Development ◽  
1982 ◽  
Vol 69 (1) ◽  
pp. 183-192
Author(s):  
Anthony L. Mescher
Keyword(s):  
Cell Cycle ◽  
Dna Synthesis ◽  
Mitotic Activity ◽  
Mitotic Index ◽  
Elevated Level ◽  
Labelling Index ◽  
Neurotrophic Control ◽  
Epimorphic Regeneration ◽  
Baseline Levels

Denervated forelimbs and contralateral innervated forelimbs of Ambystoma larvae were injured internally distal to the elbow by compression with watchmaker's forceps. Innervated controls completely repaired the crush injury within one week; denervated limbs failed to repair the injury and exhibited varying degrees of limb regression. Histological examination revealed that the process of tissue dedifferentiation initiated by injury was more extensive in denervated, regressing limbs than in controls. In innervated limbs, both the DNA labelling index and the mitotic index peaked approximately 4–6 days after the injury and returned to baseline levels by 10 days. In denervated limbs, the DNA labelling index also increased and remained at an elevated level for at least 2 weeks after the injury, but significant mitotic activity was not observed. The data indicate that intact nerves are not needed for cellular dedifferentiation, cell cycle re-entry, and DNA synthesis in injured limbs, but are required for the cells to proliferate and repair the injury. These results are discussed together with those of similar experiments on the role of nerves during the initiation of epimorphic regeneration in amputated limbs.

scholarly journals Fluctuation in radioresponse of HeLa cells during the cell cycle evaluated based on micronucleus frequency

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Hiroaki Shimono ◽  
Atsushi Kaida ◽  
Hisao Homma ◽  
Hitomi Nojima ◽  
Yusuke Onozato ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Hela Cells ◽  
Time Lapse ◽  
S Phase ◽  
G1 Phase ◽  
M Phase ◽  
G2 Phase ◽  
The Difference ◽  
Time Lapse Imaging ◽  
First Time

AbstractIn this study, we examined the fluctuation in radioresponse of HeLa cells during the cell cycle. For this purpose, we used HeLa cells expressing two types of fluorescent ubiquitination-based cell cycle indicators (Fucci), HeLa-Fucci (CA)2 and HeLa-Fucci (SA), and combined this approach with the micronucleus (MN) assay to assess radioresponse. The Fucci system distinguishes cell cycle phases based on the colour of fluorescence and cell morphology under live conditions. Time-lapse imaging allowed us to further identify sub-positions within the G1 and S phases at the time of irradiation by two independent means, and to quantitate the number of MNs by following each cell through M phase until the next G1 phase. Notably, we found that radioresponse was low in late G1 phase, but rapidly increased in early S phase. It then decreased until late S phase and increased in G2 phase. For the first time, we demonstrated the unique fluctuation of radioresponse by the MN assay during the cell cycle in HeLa cells. We discuss the difference between previous clonogenic experiments using M phase-synchronised cell populations and ours, as well as the clinical implications of the present findings.

Some evidence for replication-transcription coupling in Physarum polycephalum

1975 ◽  
Vol 18 (1) ◽  
pp. 27-39
Author(s):  
H. Fouquet ◽  
R. Bohme ◽  
R. Wick ◽  
H.W. Sauer ◽  
K. Scheller
Keyword(s):  
Cell Cycle ◽  
Dna Synthesis ◽  
Dna Sequences ◽  
Physarum Polycephalum ◽  
Rna Synthesis ◽  
Selective Inhibition ◽  
S Phase ◽  
Dna Molecules ◽  
Uridine Incorporation ◽  
G2 Phase

Hydroxyurea, at concentrations of 40–60 mM, selectively and effectively blocked incorporation of thymidine into DNA. Inhibition occurred within 5–10 min of application of the agent when DNA synthesis was in progress, while the onset of replication at the beginning of S-phase and DNA synthesis in G2 phase were not affected. Uridine incorporation into TCA-precipitable material, in the presence of hydroxyurea, was significantly (up to 70%) inhibited in early S-phase of the cell cycle. Selective inhibition of RNA synthesis was confirmed for RNA separated into rRNA-rich and poly(A)-rich RNA fractions and analysed by the 2 kinds of DNA-RNA hybridization reactions. Uridine incorporation into poly (A) RNA was also inhibited under conditions where cycloheximide prevented maturation of nascent DNA molecules in early S-phase. We assume that chromatin which is replicating early DNA sequences may be a more competent template for transcription.

scholarly journals MyoD induced cell cycle arrest is associated with increased nuclear affinity of the Rb protein.

1993 ◽  
Vol 4 (7) ◽  
pp. 705-713 ◽  
Author(s):  
A M Thorburn ◽  
P A Walton ◽  
J R Feramisco
Keyword(s):  
Cell Cycle ◽  
Tumor Suppressor ◽  
Dna Synthesis ◽  
Cell Cycle Arrest ◽  
S Phase ◽  
Tumor Suppressor Protein ◽  
G1 Phase ◽  
Induced Expression ◽  
Rb Protein ◽  
Cycle Arrest

In studying the mechanism through which the myogenic determination protein MyoD prevents entry into the S phase of the cell cycle, we have found a relationship between MyoD and the retinoblastoma (Rb) tumor suppressor protein. By direct needle microinjection of purified recombinant MyoD protein into quiescent fibroblasts, which were then induced to proliferate by serum, we found that MyoD arrested progression of the cell cycle, in agreement with studies utilizing expression constructs for MyoD. By studying temporal changes in cells injected with MyoD protein, it was found that MyoD did not prevent serum induced expression of the protooncogene c-Fos, an event that occurs in the G0 to G1 transition of the cycle. Injection of the MyoD protein as late as 8 h after the addition of serum still caused an inhibition in DNA synthesis, suggesting that MyoD inhibits the G1 to S transition as opposed to the G0 to G1 transition. MyoD injection did not prevent the expression of cyclin A. However MyoD injection did result in a block in the increase in Rb extractibility normally seen in late G1 phase cells. As this phenomenon is associated with the hyperphosphorylation of Rb at this point in the cell cycle and is correlated with progression into S phase, this provides further evidence that MyoD blocks the cycle late in G1.

scholarly journals Anti-proliferative mechanism of Huaier extract in human thyroid carcinoma cells

2020 ◽  
Author(s):  
Jingni He ◽  
Ying Zhang ◽  
Lidong Wang ◽  
Yifang Yu ◽  
Baiyu Yao ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Flow Cytometry ◽  
Thyroid Cancer ◽  
Cancer Cells ◽  
High Throughput ◽  
High Throughput Sequencing ◽  
Treated Group ◽  
G1 Phase ◽  
Thyroid Cancer Cells ◽  
Number Of Cells

Abstract BackgroundThyroid cancer is the most common endocrine tumor and typically has a good prognosis; however, some patients still present with local or distant metastases. Huaier is a traditional Chinese medicine reported as effective in treating certain types of tumor, but the effect of Huaier on thyroid cancer has not yet been reported. MethodsThe thyroid cancer cell lines, B-CPAP and C643, were treated with increasing concentrations of Huaier extract and the therapeutic effect was measured using a cell counting kit 8 (CCK-8) and flow cytometry. High-throughput sequencing was further performed to identify differentially expressed genes (DEGs) in Huaier-treated B-CPAP cells. Moreover, quantitative real-time PCR (RT-qPCR) was carried out to verify the selected RNAs. Finally, the dual luciferase detection kit was used to detect gene activity.ResultsProliferation of B-CPAP and C643 cells was significantly suppressed by treatment with Huaier extract in a concentration- and time-dependent manner. Huaier extract also induced cell cycle arrest and apoptosis according to flow cytometry (p < 0.05).High-throughput sequencing observed 7,979 significantly altered transcripts. Gene Ontology (GO) analysis showed that 270 genes were enriched in upregulated terms, while 171 genes were enriched in downregulated terms (p < 0.05). Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis indicated that there were 47 enriched pathways associated with DEGs (p < 0.05). The expression levels of chosen lncRNAs (SNHG7, MIR181A2HG, ILF3-AS1, and CTA-29F11.1) and their corresponding mRNAs (BBC3, CTSL, GADD45A, and DDIT3) were verified to be overexpressed in Huaier-treated B-CPAP cells by RT-qPCR (p < 0.05).Following transduction, the CCK-8 results showed that the proliferative capacity was increased in the shRNA group as compared with that in the Ctrl and Scr groups. According to flow cytometry, the number of cells in the G0/G1 phase was decreased in the shRNA group (p < 0.01) and the apoptosis rate was lower (p < 0.05). The shRNA-treated group had significantly reduced Huaier-induced apoptosis as compared with the Scr-treated group (p < 0.05). Moreover, the number of cells in the G0/G1 phase in the shRNA-treated group was significantly lower than that in the Scr-treated group (p < 0.05). The results of the dual luciferase reporter gene experiment showed that the activity in the GADD45A WT + miR-301a-3p(+) group was significantly reduced as compared with that in the GADD45A WT + miR-301a-3p(+) NC group (p < 0.01). Further, the activity in the ILF3-AS1 WT + miR-301a-3p(+) group was significantly lower than that in the ILF3-AS1 WT + miR-301a-3p(+) NC group (p < 0.05).ConclusionsThe present study demonstrates that Huaier extract inhibits the proliferation of thyroid cancer cells via changes in the expression levels of a multitude of genes. In particular, a decrease in GADD45A expression enhances the proliferative ability of thyroid cancer cells, the levels of which can be increased by Huaier treatment, thus regulating the cell cycle and apoptosis. Huaier can inhibit the proliferation of thyroid cancer cells through the ILF3-AS1/hsa-miR-301a-3p/GADD45A ceRNA axis.

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