scholarly journals Functions of Cyclin A1 in the Cell Cycle and Its Interactions with Transcription Factor E2F-1 and the Rb Family of Proteins

1999 ◽  
Vol 19 (3) ◽  
pp. 2400-2407 ◽  
Author(s):  
Rong Yang ◽  
Carsten Müller ◽  
Vong Huynh ◽  
Yuen K. Fung ◽  
Amy S. Yee ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Transcription Factor ◽  
Mitotic Cell ◽  
Histone H1 ◽  
Mitotic Cell Cycle ◽  
Osteosarcoma Cell ◽  
Cell Cycle Regulators ◽  
Cyclin A1 ◽  
Transcription Factor E2f

ABSTRACT Human cyclin A1, a newly discovered cyclin, is expressed in testis and is thought to function in the meiotic cell cycle. Here, we show that the expression of human cyclin A1 and cyclin A1-associated kinase activities was regulated during the mitotic cell cycle. In the osteosarcoma cell line MG63, cyclin A1 mRNA and protein were present at very low levels in cells at the G0 phase. They increased during the progression of the cell cycle and reached the highest levels in the S and G2/M phases. Furthermore, the cyclin A1-associated histone H1 kinase activity peaked at the G2/M phase. We report that cyclin A1 could bind to important cell cycle regulators: the Rb family of proteins, the transcription factor E2F-1, and the p21 family of proteins. The in vitro interaction of cyclin A1 with E2F-1 was greatly enhanced when cyclin A1 was complexed with CDK2. Associations of cyclin A1 with Rb and E2F-1 were observed in vivo in several cell lines. When cyclin A1 was coexpressed with CDK2 in sf9 insect cells, the CDK2-cyclin A1 complex had kinase activities for histone H1, E2F-1, and the Rb family of proteins. Our results suggest that the Rb family of proteins and E2F-1 may be important targets for phosphorylation by the cyclin A1-associated kinase. Cyclin A1 may function in the mitotic cell cycle in certain cells.

scholarly journals Evolutionary repair: changes in multiple functional modules allow meiotic cohesin to support mitosis

2019 ◽  
Author(s):  
Yu-Ying Phoebe Hsieh ◽  
Vasso Makrantoni ◽  
Daniel Robertson ◽  
Adèle L Marston ◽  
Andrew W Murray
Keyword(s):  
Cell Cycle ◽  
Mitotic Cell ◽  
S Phase ◽  
Genome Replication ◽  
Mitotic Cell Cycle ◽  
Functional Modules ◽  
Cell Cycle Regulators ◽  
Cellular Functions ◽  
Biochemical Activity ◽  
Sister Chromosome

AbstractDifferent members of the same protein family often perform distinct cellular functions. How much are these differing functions due to changes in a protein’s biochemical activity versus changes in other proteins? We asked how the budding yeast, Saccharomyces cerevisiae, evolves when forced to use the meiosis-specific kleisin, Rec8, instead of the mitotic kleisin, Scc1, during the mitotic cell cycle. This perturbation impairs sister chromosome linkage and reduces reproductive fitness by 45%. We evolved 15 populations for 1750 generations, substantially increasing their fitness, and analyzed their genotypes and phenotypes. We found no mutations in Rec8, but many populations had mutations in the transcriptional mediator complex, cohesin-related genes, and cell cycle regulators that induce S phase. These mutations improve sister chromosome cohesion and slow genome replication in Rec8-expressing cells. We conclude that changes in known and novel partners allow proteins to improve their ability to perform new functions.

Activation of p34cdc2 protein kinase activity in meiotic and mitotic cell cycles in mouse oocytes and embryos

Development ◽  
1991 ◽  
Vol 113 (3) ◽  
pp. 789-795 ◽  
Author(s):  
T. Choi ◽  
F. Aoki ◽  
M. Mori ◽  
M. Yamashita ◽  
Y. Nagahama ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Protein Kinase ◽  
Kinase Activity ◽  
Polar Body ◽  
Mitotic Cell ◽  
Histone H1 ◽  
Protein Kinase Activity ◽  
Mitotic Cell Cycle ◽  
Mouse Oocytes ◽  
First Polar Body

p34cdc2 protein kinase is a universal regulator of M-phase in eukaryotic cell cycle. To investigate the regulation of meiotic and mitotic cell cycle in mammals, we examined the changes in phosphorylation states of p34cdc2 and its histone H1 kinase activity in mouse oocytes and embryos. We showed that p34cdc2 has three different migrating bands (referred to as upper, middle and lower bands) on SDS-PAGE followed by immunoblotting with anti-PSTAIR antibody, and that the upper and middle bands are phosphorylated forms since these two bands shifted to the lower one by alkaline phosphatase treatment. In meiotic cell cycle, only germinal vesicle (GV) stage oocytes had the three forms. The phosphorylated forms decreased gradually in oocytes up to 2 h after isolation from follicles, and thereafter the phosphorylation states did not change significantly until metaphase II. However, the histone H1 kinase activity oscillated, being activated at the first and second metaphase in meiosis and inactivated at the time of the first polar body extrusion. These results suggest that changes in phosphorylation states of p34cdc2 triggered its activation at the first metaphase, but not inactivation and reactivation at the first and second metaphase, respectively. In mitotic cell cycle, phosphorylated forms appeared at 4 h after insemination, increased greatly just before metaphase, and were dephosphorylated in metaphase. Histone H1 kinase activity was high only at metaphase. This kinase activation is probably triggered by dephosphorylation of p34cdc2.

scholarly journals Interaction of Sp1 with the growth- and cell cycle-regulated transcription factor E2F.

1996 ◽  
Vol 16 (4) ◽  
pp. 1659-1667 ◽  
Author(s):  
J Karlseder ◽  
H Rotheneder ◽  
E Wintersberger
Keyword(s):  
Cell Cycle ◽  
Transcription Factor ◽  
Transcription Factors ◽  
Binding Sites ◽  
Promoter Activity ◽  
Binding Motif ◽  
Transcription Machinery ◽  
Transcription Factor E2f

Within the region around 150 bp upstream of the initiation codon, which was previously shown to suffice for growth-regulated expression, the murine thymidine kinase gene carries a single binding site for transcription factor Sp1; about 10 bp downstream of this site, there is a binding motif for transcription factor E2F. The latter protein appears to be responsible for growth regulation of the promoter. Mutational inactivation of either the Sp1 or the E2F site almost completely abolishes promoter activity, suggesting that the two transcription factors interact directly in delivering an activation signal to the basic transcription machinery. This was verified by demonstrating with the use of glutathione S-transferase fusion proteins that E2F and Sp1 bind to each other in vitro. For this interaction, the C-terminal part of Sp1 and the N terminus of E2F1, a domain also present in E2F2 and E2F3 but absent in E2F4 and E2F5, were essential. Accordingly, E2F1 to E2F3 but not E2F4 and E2F5 were found to bind sp1 in vitro. Coimmunoprecipitation experiments showed that complexes exist in vivo, and it was estabilished that the distance between the binding sites for the two transcription factors was critical for optimal promoter activity. Finally, in vivo footprinting experiments indicated that both the sp1 and E2F binding sites are occupied throughout the cell cycle. Mutation of either binding motif abolished binding of both transcription factors in vivo, which may indicate cooperative binding of the two proteins to chromatin-organized DNA. Our data are in line with the hypothesis that E2F functions as a growth- and cell cycle regulated tethering factor between Sp1 and the basic transcription machinery.

scholarly journals Activation of Wee1 by p42 MAPK In Vitro and in CyclingXenopus Egg Extracts

2000 ◽  
Vol 11 (3) ◽  
pp. 887-896 ◽  
Author(s):  
Sarah A. Walter ◽  
Sarah N. Guadagno ◽  
James E. Ferrell
Keyword(s):  
Cell Cycle ◽  
Mapk Pathway ◽  
Fold Increase ◽  
Mitotic Cell ◽  
Mitogen Activated Protein Kinase ◽  
Mitotic Cell Cycle ◽  
Egg Extracts ◽  
Negative Effect ◽  
G2 Phase

Xenopus oocytes and eggs provide a dramatic example of how the consequences of p42 mitogen-activated protein kinase (p42 MAPK) activation depend on the particular context in which the activation occurs. In oocytes, the activation of Mos, MEK, and p42 MAPK is required for progesterone-induced Cdc2 activation, and activated forms of any of these proteins can bring about Cdc2 activation in the absence of progesterone. However, in fertilized eggs, activation of the Mos/MEK/p42 MAPK pathway has the opposite effect, inhibiting Cdc2 activation and causing a G2 phase delay or arrest. In the present study, we have investigated the mechanism and physiological significance of the p42 MAPK-induced G2 phase arrest, usingXenopus egg extracts as a model system. We found that Wee1-depleted extracts were unable to arrest in G2 phase in response to Mos, and adding back Wee1 to the extracts restored their ability to arrest. This finding formally places Wee1 downstream of Mos/MEK/p42 MAPK. Purified recombinant p42 MAPK was found to phosphorylate recombinant Wee1 in vitro at sites that are phosphorylated in extracts. Phosphorylation by p42 MAPK resulted in a modest (∼2-fold) increase in the kinase activity of Wee1 toward Cdc2. Titration experiments in extracts demonstrated that a twofold increase in Wee1 activity is sufficient to cause the delay in mitotic entry seen in Mos-treated extracts. Finally, we present evidence that the negative regulation of Cdc2 by Mos/MEK/p42 MAPK contributes to the presence of an unusually long G2 phase in the first mitotic cell cycle. Prematurely inactivating p42 MAPK in egg extracts resulted in a corresponding hastening of the first mitosis. The negative effect of p42 MAPK on Cdc2 activation may help ensure that the first mitotic cell cycle is long enough to allow karyogamy to be accomplished successfully.

scholarly journals Heat stress tolerance assayed in four wine-producing grapevine varieties using a cytogenetic approach

2019 ◽  
Vol 34 (1) ◽  
pp. 61-70
Author(s):  
Ana Carvalho ◽  
Fernanda Leal ◽  
Manuela Matos ◽  
José Lima-Brito
Keyword(s):  
Cell Cycle ◽  
Heat Stress ◽  
Mitotic Cell ◽  
Root Tip ◽  
Mitotic Cell Cycle ◽  
Root Tips ◽  
Excessive Heat ◽  
Dividing Cells ◽  
Treatment Interaction

The degree of tolerance to heat stress (HS) differs among grapevine varieties. HS affects the duration and the regularity of the cell cycle in plants. The cytogenetic studies in grapevine are scarce, and the consequences of HS in the mitosis are barely known. This work intends to evaluate the consequences of induced HS in the mitotic cell cycle and chromosomes of four wine-producing varieties: Touriga Franca (TF), Touriga Nacional (TN), Rabigato and Viosinho using a cytogenetic approach. HS (1h at 42 ºC) was induced in plants of the four grapevine varieties that grew in vitro for 11 months. Plants of the same varieties and with equal age were used as control (maintained in vitro at 25 ºC). Three plants per variety and treatment (control and HS) were analysed. After HS, root-tips were collected in all plants and immediately fixed to be used for the preparation of mitotic chromosome spreads. In total, 6,116 root-tip cells were scored. Among the 5,973 dividing cells, 24.33% showed different types of irregularities in all mitotic phases (prophase, metaphase, anaphase, and telophase). After HS, the mitotic index (MI) decreased in the varieties TF and Viosinho, and increased in TN and Rabigato, relatively to the control. However, the average values of MI did not show statistically significant differences (p ˃ 0.05) among varieties, treatments and for the variety x treatment interaction. The percentage of dividing cells with anomalies (%DCA) increased after HS in all varieties relatively to the control. The average values of %DCA presented statistically significant differences (p < 0.05) only between treatments. As far as we know, this work constitutes the first cytogenetic evaluation of the HS effects in the mitotic cell cycle and chromosomes of grapevine using meristematic cells of root-tips. TN has been considered tolerant to various abiotic stresses (drought and excessive heat and light) based on other methodologies. TF and Viosinho have been referred as tolerant to abiotic stress without deeper studies available, and till the development of our investigation, the sensibility of Rabigato was unknown. Among the varieties analysed in this work, Rabigato revealed to be the less tolerant to HS. This research can be useful for selection of grapevine clones more tolerant to HS for commercialization and for the improvement of the economic sustainability.

scholarly journals SOG1 transcription factor promotes the onset of endoreduplication under salinity stress in Arabidopsis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Kalyan Mahapatra ◽  
Sujit Roy
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Death ◽  
Transcription Factor ◽  
Programmed Cell Death ◽  
Salinity Stress ◽  
Crucial Role ◽  
Genome Stability ◽  
Cell Cycle Checkpoint ◽  
Cell Cycle Regulators

AbstractAs like in mammalian system, the DNA damage responsive cell cycle checkpoint functions play crucial role for maintenance of genome stability in plants through repairing of damages in DNA and induction of programmed cell death or endoreduplication by extensive regulation of progression of cell cycle. ATM and ATR (ATAXIA-TELANGIECTASIA-MUTATED and -RAD3-RELATED) function as sensor kinases and play key role in the transmission of DNA damage signals to the downstream components of cell cycle regulatory network. The plant-specific NAC domain family transcription factor SOG1 (SUPPRESSOR OF GAMMA RESPONSE 1) plays crucial role in transducing signals from both ATM and ATR in presence of double strand breaks (DSBs) in the genome and found to play crucial role in the regulation of key genes involved in cell cycle progression, DNA damage repair, endoreduplication and programmed cell death. Here we report that Arabidopsis exposed to high salinity shows generation of oxidative stress induced DSBs along with the concomitant induction of endoreduplication, displaying increased cell size and DNA ploidy level without any change in chromosome number. These responses were significantly prominent in SOG1 overexpression line than wild-type Arabidopsis, while sog1 mutant lines showed much compromised induction of endoreduplication under salinity stress. We have found that both ATM-SOG1 and ATR-SOG1 pathways are involved in the salinity mediated induction of endoreduplication. SOG1was found to promote G2-M phase arrest in Arabidopsis under salinity stress by downregulating the expression of the key cell cycle regulators, including CDKB1;1, CDKB2;1, and CYCB1;1, while upregulating the expression of WEE1 kinase, CCS52A and E2Fa, which act as important regulators for induction of endoreduplication. Our results suggest that Arabidopsis undergoes endoreduplicative cycle in response to salinity induced DSBs, showcasing an adaptive response in plants under salinity stress.

Paclitaxel inhibits osteoclast formation and bone resorption via influencing mitotic cell cycle arrest and RANKL-induced activation of NF-κB and ERK

2012 ◽  
Vol 113 (3) ◽  
pp. 946-955 ◽  
Author(s):  
Estabelle S. M. Ang ◽  
Nathan J. Pavlos ◽  
Shek Man Chim ◽  
Hao Tian Feng ◽  
Robin M. Scaife ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Bone Resorption ◽  
Cell Cycle Arrest ◽  
Mitotic Cell ◽  
Osteoclast Formation ◽  
Mitotic Cell Cycle ◽  
Cycle Arrest

Anti-glioma Efficacy and Mechanism of Action of Tripolinolate A from Tripolium pannonicum

Planta Medica ◽  
2018 ◽  
Vol 84 (11) ◽  
pp. 786-794
Author(s):  
Weiyun Chai ◽  
Lu Chen ◽  
Xiao-Yuan Lian ◽  
Zhizhen Zhang
Keyword(s):  
Cell Cycle ◽  
Transcription Factors ◽  
Glioma Cells ◽  
Inhibitory Effect ◽  
Cell Cycle Regulators ◽  
Expression Levels ◽  
Multiple Tumor ◽  
Glioma Growth

AbstractTripolinolate A as a new bioactive phenolic ester was previously isolated from a halophyte of Tripolium pannonicum. However, the in vitro and in vivo anti-glioma effects and mechanism of tripolinolate A have not been investigated. This study has demonstrated that (1) tripolinolate A inhibited the proliferation of different glioma cells with IC50 values of 7.97 to 14.02 µM and had a significant inhibitory effect on the glioma growth in U87MG xenograft nude mice, (2) tripolinolate A induced apoptosis in glioma cells by downregulating the expressions of antiapoptotic proteins and arrested glioma cell cycle at the G2/M phase by reducing the expression levels of cell cycle regulators, and (3) tripolinolate A also remarkably reduced the expression levels of several glioma metabolic enzymes and transcription factors. All data together suggested that tripolinolate A had significant in vitro and in vivo anti-glioma effects and the regulation of multiple tumor-related regulators and transcription factors might be responsible for the activities of tripolinolate A against glioma.

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