scholarly journals Regulation of cell growth and division. Transcriptional regulation of cell cycle-dependent histone genes.

1988 ◽  
Vol 62 (11) ◽  
pp. 1684-1687
Author(s):  
Masaki IWABUCHI
1987 ◽  
Vol 7 (12) ◽  
pp. 4204-4210
Author(s):  
M A Osley ◽  
D Lycan

Using a Saccharomyces cerevisiae strain containing an integrated copy of an H2A-lacZ fusion gene, we screened for mutants which overexpressed beta-galactosidase as a way to identify genes which regulate transcription of the histone genes. Five recessive mutants with this phenotype were shown to contain altered regulatory genes because they had lost repression of HTA1 transcription which occurs upon inhibition of chromosome replication (D. E. Lycan, M. A. Osley, and L. Hereford, Mol. Cell. Biol. 7:614-621, 1987). Periodic transcription was affected in the mutants as well, since the HTA1 gene was transcribed during the G1 and G2 phases of the cell cycle, periods in the cell cycle when this gene is normally not expressed. A similar loss of cell cycle-dependent transcription was noted for two of the three remaining histone loci, while the HO and CDC9 genes continued to be expressed periodically. Using isolated promoter elements inserted into a heterologous cycl-lacZ fusion gene, we demonstrated that the mutations fell in genes which acted through a negative site in the TRT1 H2A-H2B promoter.


2004 ◽  
Vol 24 (22) ◽  
pp. 10036-10046 ◽  
Author(s):  
Aline Pic-Taylor ◽  
Zoulfia Darieva ◽  
Brian A. Morgan ◽  
Andrew D. Sharrocks

ABSTRACT The forkhead transcription factor Fkh2p acts in a DNA-bound complex with Mcm1p and the coactivator Ndd1p to regulate cell cycle-dependent expression of the CLB2 gene cluster in Saccharomyces cerevisiae. Here, we demonstrate that Fkh2p is a target of cyclin-dependent protein kinases and that phosphorylation of Fkh2p promotes interactions between Fkh2p and the coactivator Ndd1p. These phosphorylation-dependent changes in the Fkh2p-Ndd1p complex play an important role in the cell cycle-regulated expression of the CLB2 cluster. Our data therefore identify an important regulatory target for cyclin-dependent kinases in the cell cycle and further our molecular understanding of the key cell cycle regulatory transcription factor Fkh2p.


Nature ◽  
1975 ◽  
Vol 257 (5529) ◽  
pp. 764-767 ◽  
Author(s):  
Gary Stein ◽  
William Park ◽  
Cary Thrall ◽  
Rusty Mans ◽  
Janet Stein

DNA Repair ◽  
2018 ◽  
Vol 69 ◽  
pp. 63-72 ◽  
Author(s):  
Maryam Abbastabar ◽  
Maryam Kheyrollah ◽  
Khalil Azizian ◽  
Nazanin Bagherlou ◽  
Sadra Samavarchi Tehrani ◽  
...  

1982 ◽  
Vol 93 (2) ◽  
pp. 459-462 ◽  
Author(s):  
D R Kiino ◽  
D E Burger ◽  
P S Dannies

GH4C1 cells (CH cells) are a clonal strain of rat pituitary tumor cells which secrete prolactin. We measured intracellular prolactin at different stages of the cell cycle using flow microfluorometry. Prolactin was stained by an indirect immunocytochemical technique using fluorescein isothiocyanate (FITC)-conjugated antiserum, and DNA was stained simultaneously with propidium iodide. We found that prolactin storage in GH cells was cell-cycle dependent; prolactin storage increased as cells passed from G1 to S to G2 + M. We have shown previously that insulin and 17 beta-estradiol act synergistically to increase intracellular prolactin three- to sevenfold and slow the rate of cell growth to approximately 70% of control cells. In this study we observed that insulin and estradiol increased prolactin storage at each stage of the cell cycle but did not affect the cell-cycle distribution of the population even though cell growth was slowed. We conclude that insulin and estradiol did not increase prolactin storage by affecting the cell-cycle distribution of the population.


Cell Cycle ◽  
2007 ◽  
Vol 6 (8) ◽  
pp. 972-981 ◽  
Author(s):  
Tong Zhou ◽  
Jeff Chou ◽  
Thomas E. Mullen ◽  
Rani Elkon ◽  
Yingchun Zhou ◽  
...  

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