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Cyclin-dependent kinases are regulators and effectors of oscillations driven by a transcription factor network

ABSTRACT: Yeast cell cycle transcription dynamics in two S. cerevisae strains grown at 37Â°C: BF264-15DU (MATa ade1 his2 leu2-3, 112 trp1-1 ura3Dns, bar1) (wild type) and a mutant of the wild type strain lacking all Cdk1 activity, cdc28-4. We compared transcript levels of genes previously shown to be periodically expressed in wild-type cells (Orlando et al, 2008, Nature) to transcript levels in the absence of Cdk1 activity. Two replicate time courses from cells lacking all Cdk1 activity and one control time course from cells with wild-type Cdk1 activity are included.

ORGANISM(S): Saccharomyces cerevisiae

SUBMITTER: Laura Simmons Kovacs

PROVIDER: E-GEOD-32974 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Cyclin-dependent kinases are regulators and effectors of oscillations driven by a transcription factor network.

Simmons Kovacs Laura A LA Mayhew Michael B MB Orlando David A DA Jin Yuanjie Y Li Qingyun Q Huang Chenchen C Reed Steven I SI Mukherjee Sayan S Haase Steven B SB

Molecular cell 20120202 5

During embryonic cell cycles, B-cyclin-CDKs function as the core component of an autonomous oscillator. Current models for the cell-cycle oscillator in nonembryonic cells are slightly more complex, incorporating multiple G1, S phase, and mitotic cyclin-CDK complexes. However, periodic events persist in yeast cells lacking all S phase and mitotic B-cyclin genes, challenging the assertion that cyclin-CDK complexes are essential for oscillations. These and other results led to the proposal that a n ...[more]

PMID: 22306294

Similar Datasets

Cyclin-dependent kinases are regulators and effectors of oscillations driven by a transcription factor network

Project description:Yeast cell cycle transcription dynamics in two S. cerevisae strains grown at 37°C: BF264-15DU (MATa ade1 his2 leu2-3, 112 trp1-1 ura3Dns, bar1) (wild type) and a mutant of the wild type strain lacking all Cdk1 activity, cdc28-4. We compared transcript levels of genes previously shown to be periodically expressed in wild-type cells (Orlando et al, 2008, Nature) to transcript levels in the absence of Cdk1 activity.

2012-02-03 | GSE32974 | GEO

Sodium arsenate response of wild type and slt2 deficient cells

Project description:Wild type (BY4741) Saccharomyces cerevisiae strains and their isogenic slt2 deficient counterparts, were treated for 2 hours with sodium arsenate 100 micromolar. Control (untreated) cells were also collected. Total RNA was extracted and analyzed by microarray hybridization. The data obtained from these experiments allows to determine those genes that are regulated by Slt2 activity after arsenate treatment. The experiments was designed as follows: Four types of samples were used: untreated wild type cells, treated wild type cells, untreated slt2- cells and treated slt2- cells. 3 independent replicates were performed for each experiment.

2010-07-25 | E-GEOD-17364 | biostudies-arrayexpress

Remodelling of whole-body lipid metabolism and a diabetic-like phenotype caused by loss of hepatic CDK1 and hepatocyte division

Project description:Purpose was to identify transcriptomic changes in whole liver and isolated hepatocytes from 12 month old wild type and Cdk1 liver-specific knock-out (Cdk1 Liv-/-) mice.

2020-10-14 | GSE159498 | GEO

Loss of hepatocyte cell division leads to liver inflammation and fibrosis

Project description:Purpose was to identify transcriptomic changes in whole liver and isolated hepatocytes from 2 week old wild type and Cdk1 liver-specific knock-out (Cdk1 Liv-/-) mice.

2020-10-14 | GSE159497 | GEO

Phosphoproteome dynamics at the transition from meiosis I to meiosis II

Project description:The proteome and phosphoproteome in meiosis from metaphase I to metaphase II after synchronisation using the GALpromoter-NDT80 block-release system are presented. The phosphoproteome dynamics are presented in two contexts: 1- in a wild-type context with 10 time points at 10min intervals 2- in a Cdc28-as1 mutant (Cdk shokat allele) where 10M of 3-MB-PP1 was added in metaphase I, and with 11 time points at 5min intervals.

2024-06-16 | PXD043862 | Pride

Cdk1 controls global epigenetic landscape in embryonic stem cells

Project description:The cyclin-dependent kinase 1 (Cdk1) represents an ancient cell cycle kinase that has been conserved from yeast to humans. Cdk1 is the only essential mammalian Cdk, which drives cytokinesis by phosphorylating a large number of cellular proteins. To uncover additional functions of Cdk1, we generated a knock-in strain of mice expressing an analog-sensitive version of Cdk1 in place of wild-type Cdk1. These mice and cells derived from them allow us to investigate Cdk1 function in essentially any compartment and at any stage of development. In our study, we focused on embryonic stem (ES) cells, as this cell type expresses particularly high levels of Cdk1. Very unexpectedly, we found that in ES cells the majority of Cdk1 substrates are localized on chromatin. Cdk1 phosphorylates a large number of proteins involved in epigenetic regulation, including writers and erasers of all major histone marks. Consistent with this finding, inhibition of Cdk1 altered histone modification status of ES cells. High levels of Cdk1 in ES cells (and in induced pluripotent stem cells) phosphorylate and partially inactivate Dot1l, the histone H3 lysine 79 methyltransferase responsible for placing activating H3K79 marks on gene bodies. Decrease of Cdk1 activity during ES cell differentiation de-represses Dot1l, thereby allowing coordinated expression of differentiation genes. These analyses indicate that Cdk1 functions to maintain the epigenetic identity of ES cells.

2020-10-05 | PXD015173 | Pride

Regulation of S-phase transcription factors by Cdk1

2014-04-10 | GSE55121 | GEO

RNA-seq of cardiac-specific Cdk1 knockout mice at 4 days after experimental myocardial infarction

Project description:Biological Relevance and Intent of the Experiment: The objective of this study is to elucidate the role of Cdk1 in cardiac function, specifically its contribution to cardiomyocyte (CM) proliferation and response to injury. Using a heart-specific Cdk1 knockout mouse model, we investigate the molecular and cellular impact of Cdk1 deficiency in the context of myocardial infarction (MI). Cdk1 is known for its regulatory functions in cell cycle progression, and its absence may significantly affect cardiac repair mechanisms post-MI. This research aims to explore whether the lack of Cdk1 impairs CM regeneration or promotes maladaptive remodeling, leading to compromised cardiac function. Overview of the Experimental Workflow: We performed RNA-sequencing (RNA-seq) on heart tissue collected from both wild-type (WT) and cardiac-specific Cdk1 knockout mice subjected to experimental MI. Heart samples were collected 4 days to capture dynamic transcriptional changes associated with Cdk1 loss. Comparative transcriptomic analysis between WT and knockout samples will reveal differentially expressed genes and signaling pathways involved in cardiomyocyte proliferation, apoptosis, and fibrosis. These insights may uncover key pathways driving heart regeneration or degeneration in the absence of Cdk1.

2024-10-31 | E-MTAB-14505 | biostudies-arrayexpress

Regulation of S-phase transcription factors by Cdk1

Project description:Analysis of gene expression across the cell cycle from wild type cells, and cells expressing alleles of Yox1, Yhp1, Hcm1, and Tos4 that cannot be phosphorylated by Cdk1. Expression of S-phase and M/G1 transcripts are downregulated when phosphorylation of these factors is blocked, demonstrating that Cdk1 promotes expression of late cell cycle genes. These experiments are two-color hybridizations of RNA isolated from synchronized wild type (WT) or phosphomutant (4P) cells, compared to RNA from asyncrhonous wild type cells in mid-log phase. Wild type and mutant cells were synchronized in G1 phase, released into the cell cycle and samples collected at 15 minute intervals. Each time course was carried out in duplicate, the replicate experiment was performed as a dye swap.

2014-04-10 | E-GEOD-55121 | biostudies-arrayexpress

Mapping Replication Fork Pause Sites in S. cerevisiae

Project description:Replication forks face multiple obstacles that slow their progression. By two-dimensional gel analysis, yeast forks pause at stable DNA protein complexes, and this pausing is greatly increased in the absence of the Rrm3 helicase. We used a genome wide approach to identify 96 sites of very high DNA polymerase binding in wild type cells. Most of these binding sites were not previously identified pause sites. Rather, the most highly represented genomic category among high DNA polymerase binding sites was the open reading frames (ORFs) of highly transcribed RNA polymerase II genes. Twice as many pause sites were identified in rrm3 compared to wild type cells as pausing in this strain occurred at both highly transcribed RNA polymerase II genes and the previously identified protein DNA complexes. ORFs of highly transcribed RNA polymerase II genes are the first class of natural pause sites that are not exacerbated in rrm3 cells. We alse mapped pause sites using a second replication fork component, Rrm3-13MYC and got similar results. Genomic input (labelled with Cy3) and IP'ed DNA (labelled with Cy5) using a MYC Ab of either DNA Pol2-13MYC or Rrm3-MYC from asynchronously grown S. cerevisiae cells in rich media were hybridized to whole-genome PCR-based arrays containing ORF and intergenic regions of the entire genome (Ivery et al 2001). At least three biological replication and one technical replicate (dye swap) were performed. Log2 transformed median normalized ratios (IP/IN) were averaged for each experiment and significant peaks of either DNA Pol2 or Rrm3 association were identified

2009-06-15 | E-GEOD-16218 | biostudies-arrayexpress

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