Cell cycle regulation of<i>cdc25C</i>transcription is mediated by the periodic repression of the glutamine-rich activators NF-Y and Sp1

Zwicker, Jörk; Groß, Claudia; Lucibello, Frances C.; Truss, Mathias; Ehlert, F; Engeland, Kurt; Müller, Rolf

doi:10.1093/nar/23.19.3822

Cited by 94 publications

(96 citation statements)

References 35 publications

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“…The hypothesis that these fluctuations in mRNA levels are based, at least in part, on promoter function is supported by results from both transient transfections with various promoter/luciferase constructs and by experiments using the stably transfected cell lines. Finally, both the presence in the PLK promoter of CDE and CHR sequences similar to those found in cdc2, cyclin A, and cdc25C promoters (12,22,23), and the fact that mutations of the CDE and CHR sequences of PLK caused elevated G 1 luciferase activity, also support a role for promoter function in the control of mRNA levels.…”

Section: Discussionmentioning

confidence: 59%

“…Potential binding sites for SP1 were previously identified in the promoters of cyclin A, cdc2, and cdc25C genes (12,22). However, we did not detect cell cycle regulated binding to the GC-rich SP1 containing PLK oligonucleotide in electrophoretic mobility shift assays, nor did mutation of the SP1 site block cell cycle regulation of the promoter/luciferase construct (data not shown).…”

Section: Fig 9 Sequence Homologies Of the Cde/chr Element Of Plkmentioning

confidence: 52%

“…Identification of Cell Cycle-regulated Repressor Elements in the PLK Promoter-Zwicker et al (12,22) reported recently that transcription of SG 2 -specific genes such as cdc25C, cdc2, and cyclin A are mediated by a cell cycle-regulated repressor element (CDE) and a cell cycle gene homology region (CHR). An alignment of the PLK promoter sequence with the CDE and CHR of these S-G 2 -specific genes shows that the PLK promoter sequence is perfectly matched with the CHR consensus sequence (Fig.…”

Section: Fig 4 Activity Of Truncated Fragments Of the Plk Promotermentioning

confidence: 99%

“…The isolated regulatory region of the cdc25C promoter contains SP1 and NF-Y binding sites and CDE and CHR repressor elements (12,22,23). The CDE/CHR element of the cdc25C gene inhibits the transcription activity of the SV40 promoter (23), demonstrating that repressor elements that interfere with the basal transcription machinery will affect all promoters.…”

Section: Fig 9 Sequence Homologies Of the Cde/chr Element Of Plkmentioning

confidence: 99%

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Cell Cycle Regulation of the Human Polo-like Kinase (PLK) Promoter

Uchiumi

Longo

Ferris

1997

Journal of Biological Chemistry

119

111

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Plk (polo-like kinase) is a serine-threonine kinase that appears to function in mitotic control in mammalian cells. We demonstrated previously that PLK mRNA expression is low at the G 1 -S transition, increases during S phase, and is maximally expressed during G 2 -M. In the present study, we have cloned the human PLK gene and analyzed the structure and function of 2 kilobases of its 5 -flanking region. Using synchronized cultures of HeLa cells transfected with PLK promoter/luciferase constructs, we show that the promoter of PLK is activated at S phase and is maximal at G 2 -M phase. Using various PLK promoter/luciferase constructs, we show that three activating regions are located between 35 and 93 base pairs upstream of the transcription initiation site. We identified a repressor element (CDE/CHR) in the region of the transcription start site, and mutations within this element diminished cell cycle regulation of transcription.

show abstract

Section: Discussionmentioning

confidence: 59%

Section: Fig 9 Sequence Homologies Of the Cde/chr Element Of Plkmentioning

confidence: 52%

Section: Fig 4 Activity Of Truncated Fragments Of the Plk Promotermentioning

confidence: 99%

Section: Fig 9 Sequence Homologies Of the Cde/chr Element Of Plkmentioning

confidence: 99%

See 2 more Smart Citations

Cell Cycle Regulation of the Human Polo-like Kinase (PLK) Promoter

Uchiumi

Longo

Ferris

1997

Journal of Biological Chemistry

119

111

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“…The trypsinized cells were stained with Hoechst 33258 and sorted according to DNA content using a Becton-Dickinson FACStar Plus (Lucibello et al, 1995) Figure 2 Genomic DMS footprinting of the cdc25C promoter in sorted G 1 and G 2 fractions of WI38VA13 cells. The positions of the CDE and the NF-Y binding sites (Lucibello et al, 1995;Zwicker et al, 1995a) are indicated. In vivo footprinting was performed exactly as described (Lucibello et al, 1995;Zwicker et al, 1995b).…”

mentioning

confidence: 99%

The SV40 large T oncoprotein disrupts DNA-binding of the cell cycle-regulated transcriptional repressor CDF

1999

Self Cite

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A hallmark of neoplastic transformation by DNA tumor viruses is the deregulation of cell cycle genes. At least in some genes, this deregulation appears to be due to the oncoprotein-mediated disruption of complexes between E2F and pocket proteins and the ensuing generation of transcriptionally active free E2F. In the present study, we have analysed the e ect of the SV40 large T oncoprotein (SV-LT) on the function of a di erent cell cycle-regulated transcriptional repressor, CDF, which is the principal regulator of the cdc25C, cyclin A and cdc2 genes. As shown by genomic footprinting of sorted G 1 and G 2 cell populations, transformation by SV-LT completely abrogated protection of the CDF binding site (CDE-CHR) in the cdc25C promoter. In agreement with this observation, expression of the SV-LT in ®broblasts led to a dramatic up-regulation of the cdc25C promoter in cells synchronized in G 0 . These ®ndings indicate that the oncoprotein-mediated dissociation of the CDF repressor protein from its cognate DNA-binding site is a major mechanism in virus-induced transcriptional deregulation.

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Expression of the 1B isoforms of divalent metal transporter (DMT1) is regulated by interaction of NF‐Y with a CCAAT‐box element near the transcription start site

Paradkar

Roth

2007

Journal Cellular Physiology

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The 1B isoforms of the divalent metal transporter (DMT1) have recently been shown to be regulated transcriptionally via NF-kappaB but whether other regulatory elements are present on this promoter, however, have not been determined. Accordingly, studies were performed to delineate a minimal promoter region responsible for basal expression of these isoforms of DMT1. Promoter analysis has established that the 1B promoter is a TATA-less promoter containing a common CCAAT-box element conserved in mouse, rat, and human. Using luciferase reporter assays, it was found that mutation of this sequence leads to more than 95% reduction in the basal activity in mouse P19 cells. Using EMSA and ChIP assay, it was confirmed that NF-YA protein subunit can bind specifically to this site. Transfecting these cells with a dominant negative (DN) form of NF-YA leads to approximately 60% decrease in luciferase activity and approximately 65% decrease in 1B form of mRNA. To determine the location of the CCAAT-box in relation to the transcription start site, 5' RACE was performed. Results of these studies reveal that the CCAAT-box resides at position -6 to -2 upstream from the transcriptional start site. These data demonstrate that binding of NF-Y to this CCAAT-box domain is responsible for the basal regulation of 1B isoforms of DMT1 mRNA.

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Cell cycle regulation ofcdc25Ctranscription is mediated by the periodic repression of the glutamine-rich activators NF-Y and Sp1

Cited by 94 publications

References 35 publications

Cell Cycle Regulation of the Human Polo-like Kinase (PLK) Promoter

Cell Cycle Regulation of the Human Polo-like Kinase (PLK) Promoter

The SV40 large T oncoprotein disrupts DNA-binding of the cell cycle-regulated transcriptional repressor CDF

Expression of the 1B isoforms of divalent metal transporter (DMT1) is regulated by interaction of NF‐Y with a CCAAT‐box element near the transcription start site

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