Cell cycle and G1 cyclins
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA140799 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE29800: Lack of G1 cyclin arrest cell cycle synchronization time-course microarray in Glucose GSE29892: Alpha Factor arrest cell cycle synchronization time-course microarray in Galactose GSE29893: Alpha Factor arrest cell cycle synchronization time-course microarray in Glucose Refer to individual Series
2011-06-11 | E-GEOD-29894 | biostudies-arrayexpress
Project description:The large majority of oxidative lesions occurring in the G1 phase of the cell cycle are repaired by base excision repair (BER) rather than mismatch repair (MMR) to avoid long resections that can lead to genomic instability and cell death. However, how cells choose BER over MMR is not yet understood. Here, we show that, during G1, D-type cyclins are recruited to sites of oxidative DNA damage in a PCNA- and p21-dependent manner. In turn, in a manner that is independent on CDK4/6 activity, D-type cyclins stabilize p21, which competes through its PCNA-interacting protein (PIP) box with MMR components for their binding to PCNA. This reduces MMR activity while allowing BER. At the G1/S transition, the AMBRA1-dependent degradation of D-type cyclins renders p21 susceptible to proteolysis via SKP2 and CDT2. These timely degradation events allow the proper binding of MMR proteins to PCNA enabling the repair of DNA replication errors. Thus, the expression of D-type cyclins limit MMR in G1, whereas their degradation is necessary for proper MMR function in S. Defects in these two regulatory mechanisms promote genome instability. The mass spectrometry raw files correspond to the affinity purifications of proximity labeled (turbo-ID) PCNA and CCND1 under various conditions.
2023-01-03 | MSV000091006 | MassIVE
Project description:Two models have been put forward for cyclin-dependent kinase (Cdk) control of the cell cycle. In the qualitative model, cell cycle events are ordered by distinct substrate specificities associated with successive waves of G1, S and mitotic cyclins. Alternatively, the gradual quantitative rise of Cdk activity from G1 phase to mitosis could lead to ordered substrate phosphorylation at sequential thresholds. Here, we study the relative contributions of qualitative and quantitative Cdk control in the budding yeast S. cerevisiae. S-phase cyclins can be replaced by a single mitotic cyclin, albeit at the cost of reduced fitness. The single cyclin can in addition replace G1 cyclins to support ordered cell cycle progression, fulfilling key predictions of the quantitative model. However, single-cyclin cells fail to polarize or grow buds and thus cannot sustain proliferation. Our results suggest that budding yeast has become dependent on G1 cyclin specificity to couple cell cycle progression to essential morphogenetic events.
2021-08-23 | PXD022757 | Pride
Project description:We performed regular RNA-seq to understand G1 cyclins function in ES cells
2017-02-07 | GSE90091 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2011-06-11 | GSE29894 | GEO
Project description:A long-term goal in cancer research has been to inhibit the cell cycle in tumour cells without causing toxicity in proliferative healthy tissues. The best evidence that this is achievable is provided by CDK4/6 inhibitors, which arrest the cell cycle in G1, are well-tolerated in patients, and are effective in treating ER+/HER2- breast cancer. CDK4/6 inhibitors are effective because they arrest tumour cells more efficiently than some healthy cell types and, in addition, they affect the tumour microenvironment to enhance anti-tumour immunity. We demonstrate here another reason to explain their efficacy. Tumour cells are specifically vulnerable to CDK4/6 inhibition because during the G1 arrest, oncogenic signals drive toxic cell overgrowth. This overgrowth causes permanent cell cycle withdrawal by either preventing progression from G1 or by inducing replication stress and genotoxic damage during the subsequent S-phase and mitosis. Inhibiting or reverting oncogenic signals that converge onto mTOR can rescue this excessive growth, DNA damage and cell cycle exit in cancer cells. Conversely, inducing oncogenic signals in non-transformed cells can drive these toxic phenotypes and sensitize cells to CDK4/6 inhibition. Together, this demonstrates how oncogenic signals that have evolved to stimulate constitutive tumour growth and proliferation driven subverted to cause toxic cell growth and irreversible cell cycle exit when proliferation is halted in G1.
2023-11-17 | PXD043792 | Pride
Project description:A growing number of small molecules are becoming available to target the cell cycle machinery for the treatment of cancer and other human diseases. Consequently, a greater understanding of the factors regulating cell cycle progression becomes essential to help enhance to response of patients to these drugs. Here we identified the poorly-studied factor FAM53C as a new regulator of the G1/S transition. We first used data from the Cancer Dependency Map to identify new candidate regulators of the G1/S transition, and validated FAM53C as necessary and sufficient for this cell cycle transition. Genetic approaches showed that FAM53C acts upstream of the RB tumor suppressor. By mass spectrometry, we identified and validated DYRK1A as a kinase normally inhibited by FAM53C. DYRK1A is an upstream negative regulator of Cyclin D, which also negatively regulates RB. Fam53C knockout mice are viable but show defects in growth. Together, these experiments identify FAM53C as a regulator of DYRK1A and of cell cycle progression in G1.
2026-04-23 | PXD055829 | Pride
Project description:Toxoplasmosis caused by the Apicomplexan parasite Toxoplasma gondii is a significant health threat to immunocompromised individuals and newborns. This parasite has a complex life cycle that is well controlled to achieve optimal transmission and pathogenesis. Acute phase of the disease is caused by rapid proliferation of tachyzoites, which has a highly coordinated and tightly regulated cell cycle to allow parasite propagation. Tachyzoite cell cycle has five partially overlapping phases (G1, S, G2, M and C) with distinct gene expression patterns and cellular activities, yet the underlying regulatory mechanisms are not well understood. In this study, we show that the AP2 family transcription factor AP2Ⅺ-3 has important roles in regulating the cell cycle to progress through the G1 phase. Depletion of AP2Ⅺ-3 resulted in cell cycle retention at G1 and impaired parasite division, leading to growth inhibition of tachyzoites. RNA-Seq and CUT&Tag analyses revealed that AP2Ⅺ-3 regulates the transcription of genes involved in nucleic acid metabolism, RNA biogenesis and processing, which are consistent with the cellular activities of G1 phase in preparing biomass for cell cycle progression. Moreover, AP2XI-3 binds to the conserved DNA motif, TRP-2, a sequence widely distributed in the promoters of genes that exhibit peak expression during the G1 phase. Together, these findings underscore the essential role of AP2Ⅺ-3 in the tight regulation of the G1 phase, highlighting its potential as a therapeutic target for drug development.
2026-03-08 | GSE322715 | GEO
Project description:This experiment measured the mono-methylation of lysine 37 of histone H3 in yeast cells at various phases of the cell cycle (G1, G1/S and S).
2021-04-28 | E-MTAB-9058 | biostudies-arrayexpress
Project description:Endothelial cells derived from hESCs were separated into 4 different cell cycle phases via FACS and sequenced (i.e., early G1, late G1, G1/S, S/G2/M)
2021-01-01 | GSE159694 | GEO